expression in the *ROB1-SAT1/ROB1* was determined using the cycle threshold (ΔΔCt) method
using the average ΔCt values of the *ACT1* gene in the *ROB1-SAT1/ROB1* strain as a calibrator.
The assays were carried out three times independently, and statistical analysis was performed
using a Welch's *t*-test.

**Supporting information**

S1 Fig. Minimum-spanning tree profile of MLST data from *C. albicans* strains isolated from the airways of patients with CF. Minimum-spanning tree analysis based on MLST data from the 56 *C. albicans* clinical isolates from CF patients in addition to the 11 maternal isolates (67 strains in total). Each circle corresponds to a distinct allelic profile (DST), and the circle size corresponds to the number of isolates sharing the same DST. The circle was coded by assigning the same color to identical clades (Green, clade 4; blue, clade 1; yellow, clade 8; orange, clade 3; pink, clade 17 and red, clade10). The shaded zones between clusters of circles indicate that the clustered DSTs belong to the same clonal complex (i.e. clades). Numerals connecting the circles indicate the number of allelic differences between the DSTs.
(JPG)

S2 Fig. Chronology of isolation of *C. albicans* clinical strains from the airways of patient CF02. The number of clinical isolates (y-axis) recovered from patient CF02 on the indicated date (x-axis, month abbreviation followed by year; 16, 2016; 17, 2017) during the period ranging from December 2016 to September 2017 (x-axis) are plotted as black histograms. The strain identifiers (starting with the letters HBJ followed by a number) are numbered according to the chronology of their sampling. When more than one isolate is recovered from a given sputum sample, an additional number separated from the strain name by a dash allows to provide a unique identifier (e.g. HBJ4 strain series were all collected in April 2017, and are composed of 5 isolates identified as HBJ4-1, HBJ4-2, HBJ4-3, HBJ4-4 and HBJ4-5). Strains isolated on a given date are listed on the corresponding histogram. For more details, see S1 Table.
(JPG)

S3 Fig. Snapshots of annotated growth curves for strains HBJ6-1, HBJ6-2 and HBJ6-3 taken from TECAN Sunrise multiplate reader. Growth curves of the indicated strains (on top of each panel) generated by a TECAN Sunrise multiplate reader device display an irregular shape in stationary phase (red arrows) for strains HBJ6-1 and HBJ6-3; indicative of morphological alterations in these two isolates. The optical density at 600 nm (OD<sub>600nm</sub>, y-axis) of each culture was measured every 10 min in YPD medium at 30°C during 42 hours (x-axis) and was plotted as a function of time in hours (x-axis).
(JPG)

S4 Fig. Strain HBJ6-2 forms pseudohyphae and/or short hyphae in different filamentation-inducing media. A. Filamentous growth of strains HBJ6-2 and HBJ6-3 (indicated on top of the panels) was assessed in RPMI (upper panel) and Spider (lower panel) liquid media, at 37°C. Thawed-out cells were incubated overnight in YPD at 30°C with shaking at 150 rpm, then harvested by centrifugation, washed once in 1X PBS and diluted to OD₆₀₀ = 0.3 in Spider and RPMI liquid media. The cells were allowed to grow for up to 6 h at 37°C. Cells were imaged using a Leica DM500 microscope. Scale bar, 100 µm. B. Monospecies biofilms made by strains HBJ6-2 (middle panel) and HBJ6-3 (right panel) were allowed to grow for 24 h in DMEM medium at 37°C in polystyrene 96-well plates as described in the Materials and Methods section entitled “Dual-species biofilms of *C. albicans* and *P. aeruginosa*.”, following a protocol provided by Dr. Rebecca Hall [14,18,19]. A well devoid of *C. albicans* cells served as a
negative control (Control). Images were captured using a Leica M80 stereomicroscope.
(JPG)

**S5 Fig. Density map of heterozygous single nucleotide polymorphisms (SNPs) across the genomes of 18 C. albicans isolates serially recovered from patient CF02.** Each chromosome (colored horizontal bar, with chromosome number indicated on top of each bar) of the complete set of 18 *C. albicans* isolates serially recovered from patient CF02 was divided into 10-kb windows with colors assigned based on the number of heterozygous SNPs found between haplotypes A and B. Colors range from white (absence of heterozygous SNPs) to deep red where roughly 100 to 150 heterozygous SNPs were identified. The centromere of each chromosome is indicated with a black vertical line. The length of each chromosome is indicated by the horizontal scale bars below each chromosome depiction (kb, kilobases; Mb, megabases). The identifier of each isolate is shown on the left side of the figure. Each row represents a strain and strains are ordered according to the chronology of their isolation (i.e. oldest strain on top). The color scale of the density of heterozygous SNPs is placed on top of the figure.
(JPG)

**S6 Fig. Examination of chromosomal rearrangements among 18 C. albicans serial clinical isolates from patient CF02 using ABHet analysis of WGS data.** Plotted are allele balance at heterozygous sites (ABHet) values (y-axis) ranging from 0.0 to 1.0 at each chromosomal position (x-axis, *C. albicans* chromosomes are identified on top of the figure as ChrX, where X stands for 1, 2, 3, 4, 5, 6, 7 or R) in the genomes of the 18 clinical isolates from patient CF02 (strain identifiers are indicated on left of the figure). ABHet values are defined as the number of reference reads from individuals with heterozygous genotypes divided by the total number of reads from such individuals (see Materials and Methods). A diploid genome will be defined by an ABHet value of 0.5. A triploid strain may contain either three identical alleles (an allelic frequency of 1) or two identical alleles and one different allele (frequencies of 0.66 and 0.33). A tetraploid strain may have allelic frequencies of either 0.5 (2×2 identical alleles), 1 (4 identical alleles), or 0.25 and 0.75 (3 identical alleles and 1 different allele).
(JPG)

**S7 Fig. Filamentous growth of strain HBJ6-3 is not inhibited in the presence of *P. aeruginosa* strain PAO1.** *C. albicans* strains HBJ6-2 and HBJ6-3 were inoculated in YPD medium and *P. aeruginosa* strain PAO1 was inoculated in LB medium. Both were incubated at 37°C for 22 h. Overnight cultures of *C. albicans* and *P. aeruginosa* were washed twice in PBS then respectively diluted to 1×10⁶ cells/ml and to 2×10⁸ cells/ml in DMEM medium. One hundred µl of *C. albicans* and 10 µL of *P. aeruginosa* were mixed in 96-well plates and the final volume adjusted to 200 µl with DMEM. The plates were incubated for 22 h at 37°C with shaking at 150 rpm. *C. albicans* and *P. aeruginosa* co-cultures were imaged using a Leica DM500 microscope. Scale bar, 100 µm.
(JPG)

**S8 Fig. Strategy for the design and construction of HBJ6-2-derived ROB1<sup>G299E</sup> and ZFU3<sup>A217T</sup> heterozygous mutants.** A. and B. Agarose gel electrophoresis of PCR amplification products used for ROB1<sup>G299E</sup>-SAT1 cassette assembly. A. Lane 1, 1Kb plus DNA ladder (Thermo Scientific GeneRuler 1 kb Plus DNA Ladder); lane 2, ROB1-Frg1 amplicon migrates at 840 bp; lane 3, ROB1-Frg2 amplicon migrates at 2465 bp; lane 3, SAT1-Frg3 amplicon migrates at 1,278 bp. B. Lane 1, 1Kb plus DNA ladder (Thermo Scientific GeneRuler 1 kb Plus DNA Ladder); lane 2, Dw-Frg4 amplicon migrates at 412 bp. C. PCR products used for ZFU3<sup>A217T</sup>-HygB cassette assembly. Lane 1, 1Kb plus DNA ladder (Thermo Scientific GeneRuler 1 kb Plus DNA Ladder); lane 2, ZFU3-Frg1 amplicon migrates at 738 bp; lane 3, ZFU3-Frg2
negative control (Control). Images were captured using a Leica M80 stereomicroscope.
(JPG)

**S5 Fig. Density map of heterozygous single nucleotide polymorphisms (SNPs) across the genomes of 18 C. albicans isolates serially recovered from patient CF02.** Each chromosome (colored horizontal bar, with chromosome number indicated on top of each bar) of the complete set of 18 *C. albicans* isolates serially recovered from patient CF02 was divided into 10-kb windows with colors assigned based on the number of heterozygous SNPs found between haplotypes A and B. Colors range from white (absence of heterozygous SNPs) to deep red where roughly 100 to 150 heterozygous SNPs were identified. The centromere of each chromosome is indicated with a black vertical line. The length of each chromosome is indicated by the horizontal scale bars below each chromosome depiction (kb, kilobases; Mb, megabases). The identifier of each isolate is shown on the left side of the figure. Each row represents a strain and strains are ordered according to the chronology of their isolation (i.e. oldest strain on top). The color scale of the density of heterozygous SNPs is placed on top of the figure.
(JPG)

**S6 Fig. Examination of chromosomal rearrangements among 18 C. albicans serial clinical isolates from patient CF02 using ABHet analysis of WGS data.** Plotted are allele balance at heterozygous sites (ABHet) values (y-axis) ranging from 0.0 to 1.0 at each chromosomal position (x-axis, *C. albicans* chromosomes are identified on top of the figure as ChrX, where X stands for 1, 2, 3, 4, 5, 6, 7 or R) in the genomes of the 18 clinical isolates from patient CF02 (strain identifiers are indicated on left of the figure). ABHet values are defined as the number of reference reads from individuals with heterozygous genotypes divided by the total number of reads from such individuals (see Materials and Methods). A diploid genome will be defined by an ABHet value of 0.5. A triploid strain may contain either three identical alleles (an allelic frequency of 1) or two identical alleles and one different allele (frequencies of 0.66 and 0.33). A tetraploid strain may have allelic frequencies of either 0.5 (2×2 identical alleles), 1 (4 identical alleles), or 0.25 and 0.75 (3 identical alleles and 1 different allele).
(JPG)

**S7 Fig. Filamentous growth of strain HBJ6-3 is not inhibited in the presence of *P. aeruginosa* strain PAO1.** *C. albicans* strains HBJ6-2 and HBJ6-3 were inoculated in YPD medium and *P. aeruginosa* strain PAO1 was inoculated in LB medium. Both were incubated at 37°C for 22 h. Overnight cultures of *C. albicans* and *P. aeruginosa* were washed twice in PBS then respectively diluted to 1×10⁶ cells/ml and to 2×10⁸ cells/ml in DMEM medium. One hundred µl of *C. albicans* and 10 µL of *P. aeruginosa* were mixed in 96-well plates and the final volume adjusted to 200 µl with DMEM. The plates were incubated for 22 h at 37°C with shaking at 150 rpm. *C. albicans* and *P. aeruginosa* co-cultures were imaged using a Leica DM500 microscope. Scale bar, 100 µm.
(JPG)

**S8 Fig. Strategy for the design and construction of HBJ6-2-derived ROB1<sup>G299E</sup> and ZFU3<sup>A217T</sup> heterozygous mutants.** A. and B. Agarose gel electrophoresis of PCR amplification products used for ROB1<sup>G299E</sup>-SAT1 cassette assembly. A. Lane 1, 1Kb plus DNA ladder (Thermo Scientific GeneRuler 1 kb Plus DNA Ladder); lane 2, ROB1-Frg1 amplicon migrates at 840 bp; lane 3, ROB1-Frg2 amplicon migrates at 2465 bp; lane 3, SAT1-Frg3 amplicon migrates at 1,278 bp. B. Lane 1, 1Kb plus DNA ladder (Thermo Scientific GeneRuler 1 kb Plus DNA Ladder); lane 2, Dw-Frg4 amplicon migrates at 412 bp. C. PCR products used for ZFU3<sup>A217T</sup>-HygB cassette assembly. Lane 1, 1Kb plus DNA ladder (Thermo Scientific GeneRuler 1 kb Plus DNA Ladder); lane 2, ZFU3-Frg1 amplicon migrates at 738 bp; lane 3, ZFU3-Frg2
amplicon migrates at 1,618 bp; lane 4, *hygB*-Frg3 amplicon migrates at 2,002 bp; lane 5, Dw-Frg4 amplicon migrates at 568 bp. **D.** Overlap extension PCR to construct allele replacement cassettes for *ROB1* and *ZFU3*. Lane 1, 1kb plus DNA ladder (Thermo Scientific GeneRuler 1 kb Plus DNA Ladder); lane 2, complete allele replacement cassette *ZFU3*<sup>A217T</sup>-*HygB* after assembling PCR products presented in panel C by fusion PCR of the four DNA fragments, with an expected size of 4,777 bp; lane3, complete allele replacement cassette *ROB1*<sup>G299E</sup>-*HygB* after assembling PCR products presented in panels A and B by fusion PCR of the four DNA fragments, with an expected size of 4,866 bp. **E.** The *ROB1*<sup>G299E</sup>-*SAT1* (upper panels) and *ZFU3*<sup>A217T</sup>-*HygB* (lower panels) heterozygous mutants were constructed in the HBJ6-2 strain background (upper and lower yellow depictions on the left). The *ROB1*<sup>G299E</sup>-*SAT1* and *ZFU3*<sup>A217T</sup>-*HygB* allele replacement cassettes are integrated into strain HBJ6-2 genomic DNA through recombinational exchanges (illustarted through dashed crossed lines) taking place between the *ROB1* (left upper panel) or *ZFU3* (left lower panel) alleles and the corresponding exogenous allele replacement cassettes flanked by upstream and downstream (DW) homology regions. Markers conferring resistance to nourseothricin (upper panel, *caSAT1*, purple rectangle) and hygromycin B (lower panel, *caHygB*, blue rectangle) are illustrated flanked by their respective promoter and terminator sequences (P and T, respectively). Growth of nourseothricin- (upper middle panel, *ROB1/ROB1*<sup>G299E</sup>) and hygromicin B- (lower middle panel, *ZFU3/ZFU3*<sup>A217T</sup>) resistant transformants on selective media is followed by colony PCR analysis to screen for heterozygous mutants (right panels). Positive *ROB1/ROB1*<sup>G299E</sup> clones C1, C4 and C5 (upper right panel, yellow stars) display a PCR-amplified fragment of 1,003 bp, whereas positive *ZFU3/ZFU3*<sup>A217T</sup> clones C1-C5 (lower right panel, yellow stars) display a PCR-amplified fragment of 594. **G.** Heterozygous single nucleotide substitutions in *ROB1* and *ZFU3* were confirmed via Sanger sequencing (yellow stars) The heterozygous mutations are indicated as double peaks at the same position within the sequencing chromatograms. Forward sequencing (F, upper panels) and reverse sequencing (R, lower panels) show similar results, validating the generation of *ROB1/ROB1*<sup>G299E</sup> and *ZFU3/ZFU3*<sup>A217T</sup> HBJ6-2 mutant derivatives.

(JPG)

**S1 Table.** List of patients recruited in this study. **Patient ID**, a specific number was assigned to each patient according to the chronology of their recruitment; **Age**, patient age in years; **Sex**, patient sex (M, male; F, female); **Sampling date**, date/month/year on which sampling was performed; **Sample #**, sample number according to the chronology of sampling; **Sample from**, body area from which sample was obtained (Exp. Sputum, expectorated sputum); **Candida culture**, indicates if culture was performed and whether yeast colonies were obtained. **Candida**, isolation of *Candida* spp. using a culture-based method at the Division of Mycology, La Rabta Hospital Tunis, relying on colony growth on Sabouraud's medium supplemented with chloramphenicol and actidione, followed by chlamydosporulation testing (see **Materials and Methods**); **# of Candida isolates**, total number of *Candida* isolates from each sputum/oral/vaginal sample; **Species ID**, *Candida* species identified using MALDI ToF or ITS sequencing approaches or a combination of both; **Method**, method used for species identification; **C. albicans strain ID**, strain nomenclature according to the chronology of sampling date; **DST**, **clade**, Diploid sequence type of the isolate based on MLST data, followed by the clade to which the isolate belongs; **Aspergillus**, indicates if an *Aspergillus* species was co-isolated with *Candida* species from the same sample; **Pseudomonas**, indicates if *Pseudomonas aeruginosa* was co-isolated with *Candida* species from the same sample; **Other bacteria**, indicates if other bacteria species were co-isolated with *Candida* species from the same sample; **N/A**, not applicable; **ND**, not determined.

(XLSX)
amplicon migrates at 1,618 bp; lane 4, *hygB*-Frg3 amplicon migrates at 2,002 bp; lane 5, Dw-Frg4 amplicon migrates at 568 bp. **D.** Overlap extension PCR to construct allele replacement cassettes for *ROB1* and *ZFU3*. Lane 1, 1kb plus DNA ladder (Thermo Scientific GeneRuler 1 kb Plus DNA Ladder); lane 2, complete allele replacement cassette *ZFU3*<sup>A217T</sup>-*HygB* after assembling PCR products presented in panel C by fusion PCR of the four DNA fragments, with an expected size of 4,777 bp; lane3, complete allele replacement cassette *ROB1*<sup>G299E</sup>-*HygB* after assembling PCR products presented in panels A and B by fusion PCR of the four DNA fragments, with an expected size of 4,866 bp. **E.** The *ROB1*<sup>G299E</sup>-*SAT1* (upper panels) and *ZFU3*<sup>A217T</sup>-*HygB* (lower panels) heterozygous mutants were constructed in the HBJ6-2 strain background (upper and lower yellow depictions on the left). The *ROB1*<sup>G299E</sup>-*SAT1* and *ZFU3*<sup>A217T</sup>-*HygB* allele replacement cassettes are integrated into strain HBJ6-2 genomic DNA through recombinational exchanges (illustarted through dashed crossed lines) taking place between the *ROB1* (left upper panel) or *ZFU3* (left lower panel) alleles and the corresponding exogenous allele replacement cassettes flanked by upstream and downstream (DW) homology regions. Markers conferring resistance to nourseothricin (upper panel, *caSAT1*, purple rectangle) and hygromycin B (lower panel, *caHygB*, blue rectangle) are illustrated flanked by their respective promoter and terminator sequences (P and T, respectively). Growth of nourseothricin- (upper middle panel, *ROB1/ROB1*<sup>G299E</sup>) and hygromicin B- (lower middle panel, *ZFU3/ZFU3*<sup>A217T</sup>) resistant transformants on selective media is followed by colony PCR analysis to screen for heterozygous mutants (right panels). Positive *ROB1/ROB1*<sup>G299E</sup> clones C1, C4 and C5 (upper right panel, yellow stars) display a PCR-amplified fragment of 1,003 bp, whereas positive *ZFU3/ZFU3*<sup>A217T</sup> clones C1-C5 (lower right panel, yellow stars) display a PCR-amplified fragment of 594. **G.** Heterozygous single nucleotide substitutions in *ROB1* and *ZFU3* were confirmed via Sanger sequencing (yellow stars) The heterozygous mutations are indicated as double peaks at the same position within the sequencing chromatograms. Forward sequencing (F, upper panels) and reverse sequencing (R, lower panels) show similar results, validating the generation of *ROB1/ROB1*<sup>G299E</sup> and *ZFU3/ZFU3*<sup>A217T</sup> HBJ6-2 mutant derivatives.

(JPG)

**S1 Table.** List of patients recruited in this study. **Patient ID**, a specific number was assigned to each patient according to the chronology of their recruitment; **Age**, patient age in years; **Sex**, patient sex (M, male; F, female); **Sampling date**, date/month/year on which sampling was performed; **Sample #**, sample number according to the chronology of sampling; **Sample from**, body area from which sample was obtained (Exp. Sputum, expectorated sputum); **Candida culture**, indicates if culture was performed and whether yeast colonies were obtained. **Candida**, isolation of *Candida* spp. using a culture-based method at the Division of Mycology, La Rabta Hospital Tunis, relying on colony growth on Sabouraud's medium supplemented with chloramphenicol and actidione, followed by chlamydosporulation testing (see **Materials and Methods**); **# of Candida isolates**, total number of *Candida* isolates from each sputum/oral/vaginal sample; **Species ID**, *Candida* species identified using MALDI ToF or ITS sequencing approaches or a combination of both; **Method**, method used for species identification; **C. albicans strain ID**, strain nomenclature according to the chronology of sampling date; **DST**, **clade**, Diploid sequence type of the isolate based on MLST data, followed by the clade to which the isolate belongs; **Aspergillus**, indicates if an *Aspergillus* species was co-isolated with *Candida* species from the same sample; **Pseudomonas**, indicates if *Pseudomonas aeruginosa* was co-isolated with *Candida* species from the same sample; **Other bacteria**, indicates if other bacteria species were co-isolated with *Candida* species from the same sample; **N/A**, not applicable; **ND**, not determined.

(XLSX)
**S2 Table.** Clinical parameters of CF patients recruited in this study. **Patient ID**, a specific number was assigned to each patient according to the chronology of their recruitment; **Mutation**, CFTR mutation for each patient was provided by the group of Pr. Taieb Messaoud at Children's Hospital in Tunis. Confirmed CF diagnosis was established based on clinical symptoms with two positive sweat chloride tests, sequencing of the CFTR gene and identification of the CF-causing mutation; **BMI**, body mass index for each patient, defined as the body weight in kilograms divided by the square of height in meters; **P. aeruginosa**, colonization, chronicity of *P. aeruginosa* carriage (chronic, intermittent or undetectable); **Mucoid P. aeruginosa**, presence or absence of mucoid form of *P. aeruginosa* (Yes, presence; No, absence); **ABPA**, presence (Yes) or absence (No) of allergic bronchopulmonary aspergillosis; **Bronchiectasis**, absence (No) or presence of bronchiectasis in one, two (1 or 2 lobes) or more (≥ 2 lobes) lobes; **Burkholderia cepacia**, detection (Yes) or undetectable (No) of *Burkholderia cepacia* infection; **Respiratory exacerbation**, number of times patient was admitted in ICU for severe respiratory exacerbation; **Cirrhosis**, absence (No) or presence (Yes) of hepatic cirrhosis; **Sever-ity score**, a severity score was calculated based on arbitrary scoring scheme provided in bottom table.
(XLSX)

**S3 Table.** Primers used in this study. Includes 6 sheets listing primers used for MLST analyses (sheet #1, named MLST primers), ITS2 sequencing for species identification (sheet #2, named ITS2 primers), the generation of the *ROB1/ROB1*<sup>G299E</sup> heterozygous mutants in strain HBJ6-2 (sheet #3, named *ROB1* primers), the generation of the *ZFU3/ZFU3*<sup>A217T</sup> heterozygous mutants in strain HBJ6-2 (sheet #4, named *ZFU3* primers), the generation of *rob1Δ/rob1Δ* homozygous mutants in HBJ62 and HBJ6-3 isolates (sheet #5, named *ROB1* deletion primers) and RT-PCR and qRT-PCR analyses (sheet #6, named (q)RT-PCR primers).
(XLSX)

**S4 Table.** Complete list of single nucleotide polymorphisms across 18 isolates from patient CF02. **Chr-Position**, position of SNPs on the indicated chromosome (Ca22chrx, where x designates chromosome number, followed by position of SNP on the corresponding chromosome) according to the *C. albicans* genome Assembly 22, version A22-s07-m01-r57; **SC5314**, polymorphic nucleotide in haplotypes A and B of the reference genome; **HBJ1 to HBJ8-4**, SNPs (haplotypes A and B) relative to polymorphic nucleotide from strain SC5314 are listed for each of the 18 serially recovered clinical isolates from patient CF02.
(XLSX)

**S5 Table.** Pairwise comparison of the number of SNPs among the 18 serial isolates from patient CF02. A matrix listing the set of 18 serial isolates from patient CF02 lists the number of SNPs differentiating each isolate from the other. The average number of SNPs for each isolate when compared to each of the remaining ones is shown on the bottom of each column.
(XLSX)

**S6 Table.** List of 239 single nucleotide polymorphisms exclusively shared between strains HBJ4-3, HBJ6-1 and HBJ6-3. **Chr-Position**, position of SNPs on the indicated chromosome (Ca22chrx, where x designates chromosome number, followed by position of SNP on the corresponding chromosome) according to the *C. albicans* genome Assembly 22, version A22-s07-m01-r57; **ORF name**, systematic nomenclature of ORF, including intron or exon region, where are located differential SNPs (haplotypes A and B) in strains HBJ4-3, HBJ6-1 and HBJ6-3 relative to those present in the remaining 15 CF02 isolates; **Gene name**, name of the gene corresponding to ORF/intron/exon where the SNPs are located; **Location of SNP**, location of SNP in the genome, either in intergenic/repeat or ORF/exon/intron regions;
**S2 Table.** Clinical parameters of CF patients recruited in this study. **Patient ID**, a specific number was assigned to each patient according to the chronology of their recruitment; **Mutation**, CFTR mutation for each patient was provided by the group of Pr. Taieb Messaoud at Children's Hospital in Tunis. Confirmed CF diagnosis was established based on clinical symptoms with two positive sweat chloride tests, sequencing of the CFTR gene and identification of the CF-causing mutation; **BMI**, body mass index for each patient, defined as the body weight in kilograms divided by the square of height in meters; **P. aeruginosa**, colonization, chronicity of *P. aeruginosa* carriage (chronic, intermittent or undetectable); **Mucoid P. aeruginosa**, presence or absence of mucoid form of *P. aeruginosa* (Yes, presence; No, absence); **ABPA**, presence (Yes) or absence (No) of allergic bronchopulmonary aspergillosis; **Bronchiectasis**, absence (No) or presence of bronchiectasis in one, two (1 or 2 lobes) or more (≥ 2 lobes) lobes; **Burkholderia cepacia**, detection (Yes) or undetectable (No) of *Burkholderia cepacia* infection; **Respiratory exacerbation**, number of times patient was admitted in ICU for severe respiratory exacerbation; **Cirrhosis**, absence (No) or presence (Yes) of hepatic cirrhosis; **Sever-ity score**, a severity score was calculated based on arbitrary scoring scheme provided in bottom table.
(XLSX)

**S3 Table.** Primers used in this study. Includes 6 sheets listing primers used for MLST analyses (sheet #1, named MLST primers), ITS2 sequencing for species identification (sheet #2, named ITS2 primers), the generation of the *ROB1/ROB1*<sup>G299E</sup> heterozygous mutants in strain HBJ6-2 (sheet #3, named *ROB1* primers), the generation of the *ZFU3/ZFU3*<sup>A217T</sup> heterozygous mutants in strain HBJ6-2 (sheet #4, named *ZFU3* primers), the generation of *rob1Δ/rob1Δ* homozygous mutants in HBJ62 and HBJ6-3 isolates (sheet #5, named *ROB1* deletion primers) and RT-PCR and qRT-PCR analyses (sheet #6, named (q)RT-PCR primers).
(XLSX)

**S4 Table.** Complete list of single nucleotide polymorphisms across 18 isolates from patient CF02. **Chr-Position**, position of SNPs on the indicated chromosome (Ca22chrx, where x designates chromosome number, followed by position of SNP on the corresponding chromosome) according to the *C. albicans* genome Assembly 22, version A22-s07-m01-r57; **SC5314**, polymorphic nucleotide in haplotypes A and B of the reference genome; **HBJ1 to HBJ8-4**, SNPs (haplotypes A and B) relative to polymorphic nucleotide from strain SC5314 are listed for each of the 18 serially recovered clinical isolates from patient CF02.
(XLSX)

**S5 Table.** Pairwise comparison of the number of SNPs among the 18 serial isolates from patient CF02. A matrix listing the set of 18 serial isolates from patient CF02 lists the number of SNPs differentiating each isolate from the other. The average number of SNPs for each isolate when compared to each of the remaining ones is shown on the bottom of each column.
(XLSX)

**S6 Table.** List of 239 single nucleotide polymorphisms exclusively shared between strains HBJ4-3, HBJ6-1 and HBJ6-3. **Chr-Position**, position of SNPs on the indicated chromosome (Ca22chrx, where x designates chromosome number, followed by position of SNP on the corresponding chromosome) according to the *C. albicans* genome Assembly 22, version A22-s07-m01-r57; **ORF name**, systematic nomenclature of ORF, including intron or exon region, where are located differential SNPs (haplotypes A and B) in strains HBJ4-3, HBJ6-1 and HBJ6-3 relative to those present in the remaining 15 CF02 isolates; **Gene name**, name of the gene corresponding to ORF/intron/exon where the SNPs are located; **Location of SNP**, location of SNP in the genome, either in intergenic/repeat or ORF/exon/intron regions;
**Polymorphism**, nature of differential polymorphism in strains HBJ4-3, HBJ6-1 and HBJ6-3 relative to those present in the remaining 15 CF02 isolates; **SC5314**, polymorphic nucleotide in haplotypes A and B of the reference genome; **HBJ1 to HBJ8-4**, SNPs (haplotypes A and B) relative to polymorphic nucleotide from strain SC5314 are listed for each of the 18 serially recovered clinical isolates from patient CF02.
(XLSX)

**S7 Table. List of 34 non-synonymous single nucleotide polymorphisms exclusively shared between strains HBJ4-3, HBJ6-1 and HBJ6-3. Chr-Position**, position of non-synonymous SNPs on the indicated chromosome (Ca22chrx, where x designates chromosome number, followed by position of SNP on the corresponding chromosome) according to the *C. albicans* genome Assembly 22, version A22-s07-m01-r57; **ORF name**, systematic nomenclature of ORF where are located differential non-synonymous SNPs (haplotypes A and B) in strains HBJ4-3, HBJ6-1 and HBJ6-3 relative to SNPs present in the remaining 15 CF02 isolates; **Gene name**, name of the gene corresponding to ORF where the non-synonymous SNPs are located; **Poly-morphism**, nature of differential polymorphism in strains HBJ4-3, HBJ6-1 and HBJ6-3 relative to those present in the remaining 15 CF02 isolates; **Amino acid change**, deduced amino acid change in the predicted protein sequence of the ORF where the non-synonymous SNP from strains HBJ4-3, HBJ6-1 and HBJ6-3 is located; **SC5314**, polymorphic nucleotide in haplotypes A and B of the reference genome; **HBJ1 to HBJ8-4**, SNPs (haplotypes A and B) relative to polymorphic nucleotide from strain SC5314 are listed for each of the 18 serially recovered clinical isolates from patient CF02. The non-synonymous SNPs carried by strains HBJ4-3, HBJ6-1 and HBJ6-3 are highlighted in light gray.
(XLSX)

**S8 Table. List of C. albicans parental and mutant strains used in this study.** This table lists all parental and mutant strains used in this study, including detailed information on genotypes (column #4, relevant genotype) as well as the clone number (column #2) for each independent mutant strain generated.
(XLSX)

**Acknowledgments**

We thank Laure Lemée and Dr. Marc Monot for assistance with whole genome sequencing experiments, Dr Rebecca Hall for sharing the *C. albicans-P. aeruginosa* biofilm assay, Dr. Laurent Debarbieux for providing strain *P. aeruginosa* PAO1, Dr. Fatma Guerfali for providing access to QuantStudio 3 Real-Time PCR System and Asma Akrout, Yosr Barchouchi, Ali Bali and Wael Mami for technical assistance.

**Author Contributions**

**Conceptualization:** Sadri Znaidi.

**Formal analysis:** Mayssa Gnaien, Corinne Maufrais, Marie-Elisabeth Bougnoux, Sadri Znaidi.

**Funding acquisition:** Helmi Mardassi, Sadri Znaidi.

**Investigation:** Mayssa Gnaien, Corinne Maufrais, Yasmine Rebai, Aicha Kallel, Laurence Ma, Khaoula Meftah, Sondes Hadj Fredj, Sadri Znaidi.

**Methodology:** Sophie Bachellier-Bassi, Imène Najjar, Taieb Messaoud, Khadija Boussetta, Kalthoum Kallel, Christophe d'Enfert, Marie-Elisabeth Bougnoux, Sadri Znaidi.
**Polymorphism**, nature of differential polymorphism in strains HBJ4-3, HBJ6-1 and HBJ6-3 relative to those present in the remaining 15 CF02 isolates; **SC5314**, polymorphic nucleotide in haplotypes A and B of the reference genome; **HBJ1 to HBJ8-4**, SNPs (haplotypes A and B) relative to polymorphic nucleotide from strain SC5314 are listed for each of the 18 serially recovered clinical isolates from patient CF02.
(XLSX)

**S7 Table. List of 34 non-synonymous single nucleotide polymorphisms exclusively shared between strains HBJ4-3, HBJ6-1 and HBJ6-3. Chr-Position**, position of non-synonymous SNPs on the indicated chromosome (Ca22chrx, where x designates chromosome number, followed by position of SNP on the corresponding chromosome) according to the *C. albicans* genome Assembly 22, version A22-s07-m01-r57; **ORF name**, systematic nomenclature of ORF where are located differential non-synonymous SNPs (haplotypes A and B) in strains HBJ4-3, HBJ6-1 and HBJ6-3 relative to SNPs present in the remaining 15 CF02 isolates; **Gene name**, name of the gene corresponding to ORF where the non-synonymous SNPs are located; **Poly-morphism**, nature of differential polymorphism in strains HBJ4-3, HBJ6-1 and HBJ6-3 relative to those present in the remaining 15 CF02 isolates; **Amino acid change**, deduced amino acid change in the predicted protein sequence of the ORF where the non-synonymous SNP from strains HBJ4-3, HBJ6-1 and HBJ6-3 is located; **SC5314**, polymorphic nucleotide in haplotypes A and B of the reference genome; **HBJ1 to HBJ8-4**, SNPs (haplotypes A and B) relative to polymorphic nucleotide from strain SC5314 are listed for each of the 18 serially recovered clinical isolates from patient CF02. The non-synonymous SNPs carried by strains HBJ4-3, HBJ6-1 and HBJ6-3 are highlighted in light gray.
(XLSX)

**S8 Table. List of C. albicans parental and mutant strains used in this study.** This table lists all parental and mutant strains used in this study, including detailed information on genotypes (column #4, relevant genotype) as well as the clone number (column #2) for each independent mutant strain generated.
(XLSX)

**Acknowledgments**

We thank Laure Lemée and Dr. Marc Monot for assistance with whole genome sequencing experiments, Dr Rebecca Hall for sharing the *C. albicans-P. aeruginosa* biofilm assay, Dr. Laurent Debarbieux for providing strain *P. aeruginosa* PAO1, Dr. Fatma Guerfali for providing access to QuantStudio 3 Real-Time PCR System and Asma Akrout, Yosr Barchouchi, Ali Bali and Wael Mami for technical assistance.

**Author Contributions**

**Conceptualization:** Sadri Znaidi.

**Formal analysis:** Mayssa Gnaien, Corinne Maufrais, Marie-Elisabeth Bougnoux, Sadri Znaidi.

**Funding acquisition:** Helmi Mardassi, Sadri Znaidi.

**Investigation:** Mayssa Gnaien, Corinne Maufrais, Yasmine Rebai, Aicha Kallel, Laurence Ma, Khaoula Meftah, Sondes Hadj Fredj, Sadri Znaidi.

**Methodology:** Sophie Bachellier-Bassi, Imène Najjar, Taieb Messaoud, Khadija Boussetta, Kalthoum Kallel, Christophe d'Enfert, Marie-Elisabeth Bougnoux, Sadri Znaidi.
**Resources:** Samia Hamouda, Fatma Khalsi, Hanen Smaoui, Monia Khemiri, Taieb Messaoud, Khadija Boussetta, Kalthoum Kallel, Helmi Mardassi, Christophe d'Enfert, Marie-Elisabeth Bougnoux.

**Writing – original draft:** Mayssa Gnaien, Sadri Znaidi.

**Writing – review & editing:** Mayssa Gnaien, Corinne Maufrais, Samia Hamouda, Sophie Bachellier-Bassi, Helmi Mardassi, Christophe d'Enfert, Marie-Elisabeth Bougnoux, Sadri Znaidi.

## References

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2. Biswas L, Gotz F (2022) Molecular Mechanisms of *Staphylococcus* and *Pseudomonas* Interactions in Cystic Fibrosis. Front Cell Infect Microbiol 11: 824042.

3. Chmiel JF, Aksamit TR, Chotirmall SH, Dasenbrook EC, Elborn JS, et al. (2014) Antibiotic management of lung infections in cystic fibrosis. II. Nontuberculous mycobacteria, anaerobic bacteria, and fungi. Ann Am Thorac Soc 11: 1298–1306. https://doi.org/10.1513/AnnalsATS.201405-203AS PMID: 25167882

4. Haiko J, Saeedi B, Bagger G, Karpati F, Ozenci V (2019) Coexistence of Candida species and bacteria in patients with cystic fibrosis. Eur J Clin Microbiol Infect Dis 38: 1071–1077. https://doi.org/10.1007/s10096-019-03493-3 PMID: 30739228

5. Francis F, Enaud R, Soret P, Lussac-Sorton F, Avalos-Fernandez M, et al. (2021) New Insights in Microbial Species Predicting Lung Function Decline in CF: Lessons from the MucoFong Project. J Clin Med 10: 3725. https://doi.org/10.3390/jcm10163725 PMID: 34442021

6. Gileles-Hillel A, Shoseyov D, Polacheck I, Korem M, Kerem E, et al. (2015) Association of chronic *Candida albicans* respiratory infection with a more severe lung disease in patients with cystic fibrosis. Pediatr Pulmonol 50: 1082–1089.

7. Hector A, Chotirmall SH, Lavelle GM, Mirkovic B, Horan D, et al. (2016) Chitinase activation in patients with fungus-associated cystic fibrosis lung disease. J Allergy Clin Immunol 138: 1183–1189 e1184. https://doi.org/10.1016/j.jaci.2016.01.031 PMID: 27056270

8. Yonker LM, Marand A, Muldur S, Hopke A, Leung HM, et al. (2021) Neutrophil dysfunction in cystic fibrosis. J Cyst Fibros. 20: 1062–1071. https://doi.org/10.1016/j.jcf.2021.01.012 PMID: 33589340

9. Hopke A, Scherer A, Kreuzburg S, Abers MS, Zerbe CS, et al. (2020) Neutrophil swarming delays the growth of clusters of pathogenic fungi. Nat Commun 11: 2031. https://doi.org/10.1038/s41467-020-15834-4 PMID: 32341348

10. Kim SH, Clark ST, Surendra A, Copeland JK, Wang PW, et al. (2015) Global Analysis of the Fungal Microbiome in Cystic Fibrosis Patients Reveals Loss of Function of the Transcriptional Repressor Nrg1 as a Mechanism of Pathogen Adaptation. PLoS Pathog 11: e1005308. https://doi.org/10.1371/journal.ppat.1005308 PMID: 26588216

11. Willger SD, Grim SL, Dolben EL, Shipunova A, Hampton TH, et al. (2014) Characterization and quantification of the fungal microbiome in serial samples from individuals with cystic fibrosis. Microbiome 2: 40. https://doi.org/10.1186/2049-2618-2-40 PMID: 25408892

12. Chen Al, Dolben EF, Okegbe C, Harty CE, Golub Y, et al. (2014) *Candida albicans* ethanol stimulates *Pseudomonas aeruginosa* WspR-controlled biofilm formation as part of a cyclic relationship involving phenazines. PLoS Pathog 10: e1004480.

13. Trejo-Hernandez A, Andrade-Dominguez A, Hernandez M, Encarnacion S (2014) Interspecies competition triggers virulence and mutability in *Candida albicans*-Pseudomonas aeruginosa mixed biofilms. ISME J 8: 1974–1988.

14. Alam F, Catlow D, Di Maio A, Blair JMA, Hall RA (2020) *Candida albicans* enhances meropenem tolerance of *Pseudomonas aeruginosa* in a dual-species biofilm. J Antimicrob Chemother 75: 925–935.

15. Bliss JM, Basavegowda KP, Watson WJ, Sheikh AU, Ryan RM (2008) Vertical and horizontal transmission of *Candida albicans* in very low birth weight infants using DNA fingerprinting techniques. Pediatr Infect Dis J 27: 231–235.

16. McManus BA, Coleman DC (2014) Molecular epidemiology, phylogeny and evolution of *Candida albicans*. Infect Genet Evol 21: 166–178.
**Resources:** Samia Hamouda, Fatma Khalsi, Hanen Smaoui, Monia Khemiri, Taieb Messaoud, Khadija Boussetta, Kalthoum Kallel, Helmi Mardassi, Christophe d'Enfert, Marie-Elisabeth Bougnoux.

**Writing – original draft:** Mayssa Gnaien, Sadri Znaidi.

**Writing – review & editing:** Mayssa Gnaien, Corinne Maufrais, Samia Hamouda, Sophie Bachellier-Bassi, Helmi Mardassi, Christophe d'Enfert, Marie-Elisabeth Bougnoux, Sadri Znaidi.

## References

1. Cutting GR (2015) Cystic fibrosis genetics: from molecular understanding to clinical application. Nat Rev Genet 16: 45–56. https://doi.org/10.1038/nrg3849 PMID: 25404111

2. Biswas L, Gotz F (2022) Molecular Mechanisms of *Staphylococcus* and *Pseudomonas* Interactions in Cystic Fibrosis. Front Cell Infect Microbiol 11: 824042.

3. Chmiel JF, Aksamit TR, Chotirmall SH, Dasenbrook EC, Elborn JS, et al. (2014) Antibiotic management of lung infections in cystic fibrosis. II. Nontuberculous mycobacteria, anaerobic bacteria, and fungi. Ann Am Thorac Soc 11: 1298–1306. https://doi.org/10.1513/AnnalsATS.201405-203AS PMID: 25167882

4. Haiko J, Saeedi B, Bagger G, Karpati F, Ozenci V (2019) Coexistence of Candida species and bacteria in patients with cystic fibrosis. Eur J Clin Microbiol Infect Dis 38: 1071–1077. https://doi.org/10.1007/s10096-019-03493-3 PMID: 30739228

5. Francis F, Enaud R, Soret P, Lussac-Sorton F, Avalos-Fernandez M, et al. (2021) New Insights in Microbial Species Predicting Lung Function Decline in CF: Lessons from the MucoFong Project. J Clin Med 10: 3725. https://doi.org/10.3390/jcm10163725 PMID: 34442021

6. Gileles-Hillel A, Shoseyov D, Polacheck I, Korem M, Kerem E, et al. (2015) Association of chronic *Candida albicans* respiratory infection with a more severe lung disease in patients with cystic fibrosis. Pediatr Pulmonol 50: 1082–1089.

7. Hector A, Chotirmall SH, Lavelle GM, Mirkovic B, Horan D, et al. (2016) Chitinase activation in patients with fungus-associated cystic fibrosis lung disease. J Allergy Clin Immunol 138: 1183–1189 e1184. https://doi.org/10.1016/j.jaci.2016.01.031 PMID: 27056270

8. Yonker LM, Marand A, Muldur S, Hopke A, Leung HM, et al. (2021) Neutrophil dysfunction in cystic fibrosis. J Cyst Fibros. 20: 1062–1071. https://doi.org/10.1016/j.jcf.2021.01.012 PMID: 33589340

9. Hopke A, Scherer A, Kreuzburg S, Abers MS, Zerbe CS, et al. (2020) Neutrophil swarming delays the growth of clusters of pathogenic fungi. Nat Commun 11: 2031. https://doi.org/10.1038/s41467-020-15834-4 PMID: 32341348

10. Kim SH, Clark ST, Surendra A, Copeland JK, Wang PW, et al. (2015) Global Analysis of the Fungal Microbiome in Cystic Fibrosis Patients Reveals Loss of Function of the Transcriptional Repressor Nrg1 as a Mechanism of Pathogen Adaptation. PLoS Pathog 11: e1005308. https://doi.org/10.1371/journal.ppat.1005308 PMID: 26588216

11. Willger SD, Grim SL, Dolben EL, Shipunova A, Hampton TH, et al. (2014) Characterization and quantification of the fungal microbiome in serial samples from individuals with cystic fibrosis. Microbiome 2: 40. https://doi.org/10.1186/2049-2618-2-40 PMID: 25408892

12. Chen AI, Dolben EF, Okegbe C, Harty CE, Golub Y, et al. (2014) *Candida albicans* ethanol stimulates *Pseudomonas aeruginosa* WspR-controlled biofilm formation as part of a cyclic relationship involving phenazines. PLoS Pathog 10: e1004480.

13. Trejo-Hernandez A, Andrade-Dominguez A, Hernandez M, Encarnacion S (2014) Interspecies competition triggers virulence and mutability in *Candida albicans*-Pseudomonas aeruginosa mixed biofilms. ISME J 8: 1974–1988.

14. Alam F, Catlow D, Di Maio A, Blair JMA, Hall RA (2020) *Candida albicans* enhances meropenem tolerance of *Pseudomonas aeruginosa* in a dual-species biofilm. J Antimicrob Chemother 75: 925–935.

15. Bliss JM, Basavegowda KP, Watson WJ, Sheikh AU, Ryan RM (2008) Vertical and horizontal transmission of *Candida albicans* in very low birth weight infants using DNA fingerprinting techniques. Pediatr Infect Dis J 27: 231–235.

16. McManus BA, Coleman DC (2014) Molecular epidemiology, phylogeny and evolution of *Candida albicans*. Infect Genet Evol 21: 166–178.
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tion and trapped gas associated with genetic and environmental factors in children with cystic fibrosis.
Respir Res 7: 138. https://doi.org/10.1186/1465-9921-7-138 PMID: 17137500

18. Alam F, Blackburn SA, Davis J, Massar K, Correia J, et al. (2023) *Pseudomonas aeruginosa* increases the susceptibility of *Candida albicans* to amphotericin B in dual-species biofilms. J Antimicrob Chemother. 78: 2228-2241.

19. Alam F, Blair JMA, Hall RA (2023) Transcriptional profiling of *Pseudomonas aeruginosa* mature single- and dual-species biofilms in response to meropenem. Microbiology (Reading) 169: 001271.

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24. Glazier VE, Murante T, Koselny K, Murante D, Esqueda M, et al. (2018) Systematic Complex Haploin-
sufficiency-Based Genetic Analysis of *Candida albicans* Transcription Factors: Tools and Applications
to Virulence-Associated Phenotypes. G3 (Bethesda) 8: 1299-1314.

25. Vandeputte P, Ischer F, Sanglard D, Coste AT (2011) In Vivo Systematic Analysis of *Candida albicans*
Zn2-Cys6 Transcription Factors Mutants for Mice Organ Colonization. PLoS One 6: e26962.

26. Dorrity MW, Cuperus JT, Carlisle JA, Fields S, Queitsch C (2018) Preferences in a trait decision determined by transcription factor variants. Proc Natl Acad Sci U S A 115: E7997-E8006. https://doi.org/10.1073/pnas.1805882115 PMID: 30068600

27. Ottilie S, Luth MR, Hellemann E, Goldgof GM, Vigil E, et al. (2022) Adaptive laboratory evolution in S. cerevisiae highlights role of transcription factors in fungal xenobiotic resistance. Commun Biol 5: 128.

28. MacPherson S, Larochelle M, Turcotte B (2006) A fungal family of transcriptional regulators: the zinc cluster proteins. Microbiol Mol Biol Rev 70: 583-604. https://doi.org/10.1128/MMBR.00015-06 PMID: 16959962

29. Glazier VE, Kramara J, Ollinger T, Solis NV, Zarnowski R, et al. (2023) The *Candida albicans* refer-
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filamentation, biofilm formation, and oral commensalism. mBio: 14: e0152123.

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21. Glazier VE, Murante T, Murante D, Koselny K, Liu Y, et al. (2017) Genetic analysis of the *Candida albicans* biofilm transcription factor network using simple and complex haploinsufficiency. PLoS Genet 13: e1006948.

22. Nobile CJ, Fox EP, Nett JE, Sorrells TR, Mitrovich QM, et al. (2012) A recently evolved transcriptional network controls biofilm development in *Candida albicans*. Cell 148: 126-138.

23. Wakade RS, Ristow LC, Wellington M, Krysan DJ (2023) Intravital imaging-based genetic screen reveals the transcriptional network governing *Candida albicans* filamentation during mammalian infection. Elife 12: e85114.

24. Glazier VE, Murante T, Koselny K, Murante D, Esqueda M, et al. (2018) Systematic Complex Haploin-
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25. Vandeputte P, Ischer F, Sanglard D, Coste AT (2011) In Vivo Systematic Analysis of *Candida albicans*
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26. Dorrity MW, Cuperus JT, Carlisle JA, Fields S, Queitsch C (2018) Preferences in a trait decision determined by transcription factor variants. Proc Natl Acad Sci U S A 115: E7997-E8006. https://doi.org/10.1073/pnas.1805882115 PMID: 30068600

27. Ottilie S, Luth MR, Hellemann E, Goldgof GM, Vigil E, et al. (2022) Adaptive laboratory evolution in S. cerevisiae highlights role of transcription factors in fungal xenobiotic resistance. Commun Biol 5: 128.

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32. Gammelsrud KW, Lindstad BL, Gaustad P, Ingebretsen A, Hoiby EA, et al. (2012) Multilocus sequence typing of serial *Candida albicans* isolates from children with cancer, children with cystic fibrosis and healthy controls. Med Mycol 50: 619-626.

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34. Chen KW, Chen YC, Lo HJ, Odds FC, Wang TH, et al. (2006) Multilocus sequence typing for analyses of clonality of *Candida albicans* strains in Taiwan. J Clin Microbiol 44: 2172-2178.

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58. Crocker AW, Harty CE, Hammond JH, Willger SD, Salazar P, et al. (2019) *Pseudomonas aeruginosa* Ethanol Oxidation by AdhA in Low-Oxygen Environments. J Bacteriol 201: e00393-19.

59. O'Brien TJ, Welch M (2019) A Continuous-Flow Model for *in vitro* Cultivation of Mixed Microbial Populations Associated With Cystic Fibrosis Airway Infections. Front Microbiol 10: 2713.

60. Sriramulu DD, Lunsdorf H, Lam JS, Romling U (2005) Microcolony formation: a novel biofilm model of *Pseudomonas aeruginosa* for the cystic fibrosis lung. J Med Microbiol 54: 667-676.

61. Kasetty S, Mould DL, Hogan DA, Nadell CD (2021) Both *Pseudomonas aeruginosa* and *Candida albicans* Accumulate Greater Biomass in Dual-Species Biofilms under Flow. mSphere 6: e0041621.

62. Mukherjee PK, Chand DV, Chandra J, Anderson JM, Ghannoum MA (2009) Shear stress modulates the thickness and architecture of *Candida albicans* biofilms in a phase-dependent manner. Mycoses 52: 440-446.

63. Holland LM, Schroder MS, Turner SA, Taff H, Andes D, et al. (2014) Comparative phenotypic analysis of the major fungal pathogens Candida parapsilosis and *Candida albicans*. PLoS Pathog 10: e1004365.
64. Mancera E, Nocedal I, Hammel S, Gulati M, Mitchell KF, et al. (2021) Evolution of the complex transcription network controlling biofilm formation in *Candida* species. *Elife* 10: e64682.

65. Tseng YK, Chen YC, Hou CJ, Deng FS, Liang SH, et al. (2020) Evaluation of Biofilm Formation in *Candida tropicalis* Using a Silicone-Based Platform with Synthetic Urine Medium. *Microorganisms* 8: 660.

66. Fitzpatrick DA, O'Gaora P, Byrne KP, Butler G (2010) Analysis of gene evolution and metabolic pathways using the Candida Gene Order Browser. BMC Genomics 11: 290. https://doi.org/10.1186/1471-2164-11-290 PMID: 20459735

67. Maguire SL, OhEigeartaigh SS, Byrne KP, Schroder MS, O'Gaora P, et al. (2013) Comparative genome analysis and gene finding in *Candida* species using CGOB. Mol Biol Evol 30: 1281-1291.

68. Nguyen NH, Suh SO, Marshall CJ, Blackwell M (2006) Morphological and ecological similarities: wood-boring beetles associated with novel xylose-fermenting yeasts, *Spathaspora passalidarum* gen. sp. nov. and *Candida jeffriesii* sp. nov. Mycol Res 110: 1232-1241.

69. Cassandri M, Smirnov A, Novelli F, Pitolli C, Agostini M, et al. (2017) Zinc-finger proteins in health and disease. Cell Death Discov 3: 17071. https://doi.org/10.1038/cddiscovery.2017.71 PMID: 29152378

70. Poch O (1997) Conservation of a putative inhibitory domain in the GAL4 family members. Gene 184: 229-235. https://doi.org/10.1016/s0378-1119(96)00602-6 PMID: 9031633

71. Akache B, MacPherson S, Sylvain MA, Turcotte B (2004) Complex interplay among regulators of drug resistance genes in *Saccharomyces cerevisiae*. Journal of Biological Chemistry 279: 27855-27860.

72. King DA, Zhang L, Guarente L, Marmorstein R (1999) Structure of a HAP1-DNA complex reveals dramatically asymmetric DNA binding by a homodimeric protein. Nat Struct Biol 6: 64-71. https://doi.org/10.1038/4940 PMID: 9886294

73. Mamnun YM, Pandjaitan R, Mahe Y, Delahodde A, Kuchler K (2002) The yeast zinc finger regulators Pdr1p and Pdr3p control pleiotropic drug resistance (PDR) as homo- and heterodimers in vivo. Molecular Microbiology 46: 1429-1440. https://doi.org/10.1046/j.1365-2958.2002.03262.x PMID: 12453227

74. Noble SM, Johnson AD (2005) Strains and strategies for large-scale gene deletion studies of the diploid human fungal pathogen *Candida albicans*. Eukaryot Cell 4: 298-309.

75. Schubert S, Barker KS, Znaidi S, Schneider S, Dierolf F, et al. (2011) Regulation of efflux pump expression and drug resistance by the transcription factors Mrr1, Upc2, and Cap1 in *Candida albicans*. Antimicrob Agents Chemother 55: 2212-2223.

76. Znaidi S, De Deken X, Weber S, Rigby T, Nantel A, et al. (2007) The zinc cluster transcription factor Tac1p regulates PDR16 expression in Candida albicans. Mol Microbiol 66: 440-452.

77. Znaidi S, Weber S, Al-Abdin OZ, Bomme P, Saidane S, et al. (2008) Genomewide location analysis of *Candida albicans* Upc2p, a regulator of sterol metabolism and azole drug resistance. Eukaryot Cell 7: 836-847.

78. Morschhauser J (2009) Regulation of multidrug resistance in pathogenic fungi. Fungal Genet Biol 47: 94-106. https://doi.org/10.1016/j.fgb.2009.08.002 PMID: 19665571

79. Sanglard D, Coste A, Ferrari S (2009) Antifungal drug resistance mechanisms in fungal pathogens from the perspective of transcriptional gene regulation. FEMS Yeast Res 9: 1029-1050. https://doi.org/10.1111/j.1567-1364.2009.00578.x PMID: 19799636

80. Des Etages SA, Saxena D, Huang HL, Falvey DA, Barber D, et al. (2001) Conformational changes play a role in regulating the activity of the proline utilization pathway-specific regulator in *Saccharomyces cerevisiae*. Molecular Microbiology 40: 890-899.

81. Gregori C, Schuller C, Frohner IE, Ammerer G, Kuchler K (2008) Weak organic acids trigger conformational changes of the yeast transcription factor War1 *in vivo* to elicit stress adaptation. J Biol Chem 283: 25752-25764.

82. Wang D, Hu Y, Zheng F, Zhou K, Kohlhaw GB (1997) Evidence that intramolecular interactions are involved in masking the activation domain of transcriptional activator Leu3p. J Biol Chem 272: 19383-19392. https://doi.org/10.1074/jbc.272.31.19383 PMID: 9235937

83. Wang D, Zheng F, Holmberg S, Kohlhaw GB (1999) Yeast transcriptional regulator Leu3p. Self-mask- ing, specificity of masking, and evidence for regulation by the intracellular level of Leu3p. J Biol Chem 274: 19017-19024. https://doi.org/10.1074/jbc.274.27.19017 PMID: 10383402

84. Campbell RN, Leverentz MK, Ryan LA, Reece RJ (2008) Metabolic control of transcription: paradigms and lessons from *Saccharomyces cerevisiae*. Biochem J 414: 177-187.

85. Sellick CA, Reece RJ (2003) Modulation of transcription factor function by an amino acid: activation of Put3p by proline. EMBO J 22: 5147-5153. https://doi.org/10.1093/emboj/cdg480 PMID: 14517252

86. Sellick CA, Reece RJ (2005) Eukaryotic transcription factors as direct nutrient sensors. Trends Bio-chemSci 30: 405-412. https://doi.org/10.1016/j.tibs.2005.05.007 PMID: 15950477
64. Mancera E, Nocedal I, Hammel S, Gulati M, Mitchell KF, et al. (2021) Evolution of the complex transcription network controlling biofilm formation in *Candida* species. *Elife* 10: e64682.

65. Tseng YK, Chen YC, Hou CJ, Deng FS, Liang SH, et al. (2020) Evaluation of Biofilm Formation in *Candida tropicalis* Using a Silicone-Based Platform with Synthetic Urine Medium. *Microorganisms* 8: 660.

66. Fitzpatrick DA, O'Gaora P, Byrne KP, Butler G (2010) Analysis of gene evolution and metabolic pathways using the Candida Gene Order Browser. BMC Genomics 11: 290. https://doi.org/10.1186/1471-2164-11-290 PMID: 20459735

67. Maguire SL, OhEigeartaigh SS, Byrne KP, Schroder MS, O'Gaora P, et al. (2013) Comparative genome analysis and gene finding in *Candida* species using CGOB. Mol Biol Evol 30: 1281-1291.

68. Nguyen NH, Suh SO, Marshall CJ, Blackwell M (2006) Morphological and ecological similarities: wood-boring beetles associated with novel xylose-fermenting yeasts, *Spathaspora passalidarum* gen. sp. nov. and *Candida jeffriesii* sp. nov. Mycol Res 110: 1232-1241.

69. Cassandri M, Smirnov A, Novelli F, Pitolli C, Agostini M, et al. (2017) Zinc-finger proteins in health and disease. Cell Death Discov 3: 17071. https://doi.org/10.1038/cddiscovery.2017.71 PMID: 29152378

70. Poch O (1997) Conservation of a putative inhibitory domain in the GAL4 family members. Gene 184: 229-235. https://doi.org/10.1016/s0378-1119(96)00602-6 PMID: 9031633

71. Akache B, MacPherson S, Sylvain MA, Turcotte B (2004) Complex interplay among regulators of drug resistance genes in *Saccharomyces cerevisiae*. Journal of Biological Chemistry 279: 27855-27860.

72. King DA, Zhang L, Guarente L, Marmorstein R (1999) Structure of a HAP1-DNA complex reveals dramatically asymmetric DNA binding by a homodimeric protein. Nat Struct Biol 6: 64-71. https://doi.org/10.1038/4940 PMID: 9886294

73. Mamnun YM, Pandjaitan R, Mahe Y, Delahodde A, Kuchler K (2002) The yeast zinc finger regulators Pdr1p and Pdr3p control pleiotropic drug resistance (PDR) as homo- and heterodimers in vivo. Molecular Microbiology 46: 1429-1440. https://doi.org/10.1046/j.1365-2958.2002.03262.x PMID: 12453227

74. Noble SM, Johnson AD (2005) Strains and strategies for large-scale gene deletion studies of the diploid human fungal pathogen *Candida albicans*. Eukaryot Cell 4: 298-309.

75. Schubert S, Barker KS, Znaidi S, Schneider S, Dierolf F, et al. (2011) Regulation of efflux pump expression and drug resistance by the transcription factors Mrr1, Upc2, and Cap1 in *Candida albicans*. Antimicrob Agents Chemother 55: 2212-2223.

76. Znaidi S, De Deken X, Weber S, Rigby T, Nantel A, et al. (2007) The zinc cluster transcription factor Tac1p regulates PDR16 expression in Candida albicans. Mol Microbiol 66: 440-452.

77. Znaidi S, Weber S, Al-Abdin OZ, Bomme P, Saidane S, et al. (2008) Genomewide location analysis of *Candida albicans* Upc2p, a regulator of sterol metabolism and azole drug resistance. Eukaryot Cell 7: 836-847.

78. Morschhauser J (2009) Regulation of multidrug resistance in pathogenic fungi. Fungal Genet Biol 47: 94-106. https://doi.org/10.1016/j.fgb.2009.08.002 PMID: 19665571

79. Sanglard D, Coste A, Ferrari S (2009) Antifungal drug resistance mechanisms in fungal pathogens from the perspective of transcriptional gene regulation. FEMS Yeast Res 9: 1029-1050. https://doi.org/10.1111/j.1567-1364.2009.00578.x PMID: 19799636

80. Des Etages SA, Saxena D, Huang HL, Falvey DA, Barber D, et al. (2001) Conformational changes play a role in regulating the activity of the proline utilization pathway-specific regulator in *Saccharomyces cerevisiae*. Molecular Microbiology 40: 890-899.

81. Gregori C, Schuller C, Frohner IE, Ammerer G, Kuchler K (2008) Weak organic acids trigger conformational changes of the yeast transcription factor War1 *in vivo* to elicit stress adaptation. J Biol Chem 283: 25752-25764.

82. Wang D, Hu Y, Zheng F, Zhou K, Kohlhaw GB (1997) Evidence that intramolecular interactions are involved in masking the activation domain of transcriptional activator Leu3p. J Biol Chem 272: 19383-19392. https://doi.org/10.1074/jbc.272.31.19383 PMID: 9235937

83. Wang D, Zheng F, Holmberg S, Kohlhaw GB (1999) Yeast transcriptional regulator Leu3p. Self-mask- ing, specificity of masking, and evidence for regulation by the intracellular level of Leu3p. J Biol Chem 274: 19017-19024. https://doi.org/10.1074/jbc.274.27.19017 PMID: 10383402

84. Campbell RN, Leverentz MK, Ryan LA, Reece RJ (2008) Metabolic control of transcription: paradigms and lessons from *Saccharomyces cerevisiae*. Biochem J 414: 177-187.

85. Sellick CA, Reece RJ (2003) Modulation of transcription factor function by an amino acid: activation of Put3p by proline. EMBO J 22: 5147-5153. https://doi.org/10.1093/emboj/cdg480 PMID: 14517252

86. Sellick CA, Reece RJ (2005) Eukaryotic transcription factors as direct nutrient sensors. Trends Bio-chemSci 30: 405-412. https://doi.org/10.1016/j.tibs.2005.05.007 PMID: 15950477
87. Thakur JK, Arthanari H, Yang F, Pan SJ, Fan X, et al. (2008) A nuclear receptor-like pathway regulating multidrug resistance in fungi. *Nature* 452: 604–609. https://doi.org/10.1038/nature06836 PMID: 18385733

88. Zhang L, Hach A (1999) Molecular mechanism of heme signaling in yeast: the transcriptional activator Hap1 serves as the key mediator. *Cell MolLife Sci* 56: 415–426. https://doi.org/10.1007/s000180050442 PMID: 11212295

89. Gao C, Wang L, Milgrom E, Shen WC (2004) On the mechanism of constitutive Pdr1 activator-mediated PDR5 transcription in Saccharomyces cerevisiae: evidence for enhanced recruitment of coactivators and altered nucleosome structures. *J Biol Chem* 279: 42677–42686. https://doi.org/10.1074/jbc.M406363200 PMID: 15294907

90. Gill G, Sadowski I, Ptashne M (1990) Mutations that increase the activity of a transcriptional activator in yeast and mammalian cells. *Proc Natl Acad Sci USA* 87: 2127–2131. https://doi.org/10.1073/pnas.87.6.2127 PMID: 2179950

91. Davies BS, Wang HS, Rine J (2005) Dual activators of the sterol biosynthetic pathway of *Saccharomyces cerevisiae*: similar activation/regulatory domains but different response mechanisms. *Mol Cell Biol* 25: 7375–7385.

92. Cui L, Morris A, Ghedin E (2013) The human mycobiome in health and disease. *Genome Med* 5: 63. https://doi.org/10.1186/gm467 PMID: 23899327

93. Bougnoux ME, Tavanti A, Bouchier C, Gow NA, Magnier A, et al. (2003) Collaborative consensus for optimized multilocus sequence typing of *Candida albicans*. *J Clin Microbiol* 41: 5265–5266.

94. Liu D, Coloe S, Baird R, Pederson J (2000) Rapid mini-preparation of fungal DNA for PCR. *J Clin Microbiol* 38: 471. https://doi.org/10.1128/JCM.38.1.471-471.2000 PMID: 10681211

95. Ericson E, Hoon S, St Onge RP, Giaever G, Nislow C (2010) Exploring gene function and drug action using chemogenomic dosage assays. *Methods Enzymol* 470: 233–255. https://doi.org/10.1016/S0076-6879(10)70010-0 PMID: 20946813

96. St Onge RP, Mani R, Oh J, Proctor M, Fung E, et al. (2007) Systematic pathway analysis using high-resolution fitness profiling of combinatorial gene deletions. *Nat Genet* 39: 199–206. https://doi.org/10.1038/ng1948 PMID: 17206143

97. Ramage G, Vandewalle K, Wickes BL, Lopez-Ribot JL (2001) Characteristics of biofilm formation by *Candida albicans*. *Rev Iberoam Micol* 18: 163–170.

98. Amberg DC, Burke DJ, Strathern JN (2006) Isolation of yeast genomic DNA for southern blot analysis. *CSH Protoc* 2006: pdb.prot4149. https://doi.org/10.1101/pdb.prot4149 PMID: 22485550

99. Najjar I, Motreff L, Ma L, Lemee L, Briolat V, et al. (2021) How Did Institut Pasteur's NGS Core Facility, Biomics, Manage the Coronavirus Disease 2019 Crisis? *J Biomol Tech* 32: 50–56. https://doi.org/10.7171/jbt.21-3202-004 PMID: 34140839

100. Marton T, Maufrais C, d'Enfert C, Legrand M (2020) Use of CRISPR-Cas9 To Target Homologous Recombination Limits Transformation-Induced Genomic Changes in *Candida albicans*. *mSphere* 5: e00620–20.

101. Muzzey D, Schwartz K, Weissman JS, Sherlock G (2013) Assembly of a phased diploid *Candida albicans* genome facilitates allele-specific measurements and provides a simple model for repeat and indel structure. *Genome Biol* 14: R97.

102. Skrzypek MS, Binkley J, Binkley G, Miyasato SR, Simison M, et al. (2017) The *Candida* Genome Database (CGD): incorporation of Assembly 22, systematic identifiers and visualization of high throughput sequencing data. *Nucleic Acids Res* 45: D592–D596.

103. Li H (2021) New strategies to improve minimap2 alignment accuracy. *Bioinformatics* 37: 4572–4574. https://doi.org/10.1093/bioinformatics/btab705 PMID: 34623391

104. Van der Auwera GA, Carneiro MO, Hartl C, Poplin R, Del Angel G, et al. (2013) From FastQ data to high confidence variant calls: the Genome Analysis Toolkit best practices pipeline. *Curr Protoc Bioinformatics* 43: 11 10 11–11 10 33. https://doi.org/10.1002/0471250953.bi1110s43 PMID: 25431634

105. Thorvaldsdottir H, Robinson JT, Mesirov JP (2012) Integrative Genomics Viewer (IGV): high-performance genomics data visualization and exploration. *Brief Bioinform* 14: 178–92. https://doi.org/10.1093/bib/bbs017 PMID: 22517427

106. Loll-Krippleber R, d'Enfert C, Feri A, Diogo D, Perin A, et al. (2014) A study of the DNA damage checkpoint in *Candida albicans*: uncoupling of the functions of Rad53 in DNA repair, cell cycle regulation and genotoxic stress-induced polarized growth. *Mol Microbiol* 91: 452–471.

107. Walther A, Wendland J (2003) An improved transformation protocol for the human fungal pathogen *Candida albicans*. *Curr Genet* 42: 339–343.
87. Thakur JK, Arthanari H, Yang F, Pan SJ, Fan X, et al. (2008) A nuclear receptor-like pathway regulating multidrug resistance in fungi. *Nature* 452: 604–609. https://doi.org/10.1038/nature06836 PMID: 18385733

88. Zhang L, Hach A (1999) Molecular mechanism of heme signaling in yeast: the transcriptional activator Hap1 serves as the key mediator. *Cell MolLife Sci* 56: 415–426. https://doi.org/10.1007/s000180050442 PMID: 11212295

89. Gao C, Wang L, Milgrom E, Shen WC (2004) On the mechanism of constitutive Pdr1 activator-mediated PDR5 transcription in Saccharomyces cerevisiae: evidence for enhanced recruitment of coactivators and altered nucleosome structures. *J Biol Chem* 279: 42677–42686. https://doi.org/10.1074/jbc.M406363200 PMID: 15294907

90. Gill G, Sadowski I, Ptashne M (1990) Mutations that increase the activity of a transcriptional activator in yeast and mammalian cells. *Proc Natl Acad Sci USA* 87: 2127–2131. https://doi.org/10.1073/pnas.87.6.2127 PMID: 2179950

91. Davies BS, Wang HS, Rine J (2005) Dual activators of the sterol biosynthetic pathway of *Saccharomyces cerevisiae*: similar activation/regulatory domains but different response mechanisms. *Mol Cell Biol* 25: 7375–7385.

92. Cui L, Morris A, Ghedin E (2013) The human mycobiome in health and disease. *Genome Med* 5: 63. https://doi.org/10.1186/gm467 PMID: 23899327

93. Bougnoux ME, Tavanti A, Bouchier C, Gow NA, Magnier A, et al. (2003) Collaborative consensus for optimized multilocus sequence typing of *Candida albicans*. *J Clin Microbiol* 41: 5265–5266.

94. Liu D, Coloe S, Baird R, Pederson J (2000) Rapid mini-preparation of fungal DNA for PCR. *J Clin Microbiol* 38: 471. https://doi.org/10.1128/JCM.38.1.471-471.2000 PMID: 10681211

95. Ericson E, Hoon S, St Onge RP, Giaever G, Nislow C (2010) Exploring gene function and drug action using chemogenomic dosage assays. *Methods Enzymol* 470: 233–255. https://doi.org/10.1016/S0076-6879(10)70010-0 PMID: 20946813

96. St Onge RP, Mani R, Oh J, Proctor M, Fung E, et al. (2007) Systematic pathway analysis using high-resolution fitness profiling of combinatorial gene deletions. *Nat Genet* 39: 199–206. https://doi.org/10.1038/ng1948 PMID: 17206143

97. Ramage G, Vandewalle K, Wickes BL, Lopez-Ribot JL (2001) Characteristics of biofilm formation by *Candida albicans*. *Rev Iberoam Micol* 18: 163–170.

98. Amberg DC, Burke DJ, Strathern JN (2006) Isolation of yeast genomic DNA for southern blot analysis. *CSH Protoc* 2006: pdb.prot4149. https://doi.org/10.1101/pdb.prot4149 PMID: 22485550

99. Najjar I, Motreff L, Ma L, Lemee L, Briolat V, et al. (2021) How Did Institut Pasteur's NGS Core Facility, Biomics, Manage the Coronavirus Disease 2019 Crisis? *J Biomol Tech* 32: 50–56. https://doi.org/10.7171/jbt.21-3202-004 PMID: 34140839

100. Marton T, Maufrais C, d'Enfert C, Legrand M (2020) Use of CRISPR-Cas9 To Target Homologous Recombination Limits Transformation-Induced Genomic Changes in *Candida albicans*. *mSphere* 5: e00620–20.

101. Muzzey D, Schwartz K, Weissman JS, Sherlock G (2013) Assembly of a phased diploid *Candida albicans* genome facilitates allele-specific measurements and provides a simple model for repeat and indel structure. *Genome Biol* 14: R97.

102. Skrzypek MS, Binkley J, Binkley G, Miyasato SR, Simison M, et al. (2017) The *Candida* Genome Database (CGD): incorporation of Assembly 22, systematic identifiers and visualization of high throughput sequencing data. *Nucleic Acids Res* 45: D592–D596.

103. Li H (2021) New strategies to improve minimap2 alignment accuracy. *Bioinformatics* 37: 4572–4574. https://doi.org/10.1093/bioinformatics/btab705 PMID: 34623391

104. Van der Auwera GA, Carneiro MO, Hartl C, Poplin R, Del Angel G, et al. (2013) From FastQ data to high confidence variant calls: the Genome Analysis Toolkit best practices pipeline. *Curr Protoc Bioinformatics* 43: 11 10 11–11 10 33. https://doi.org/10.1002/0471250953.bi1110s43 PMID: 25431634

105. Thorvaldsdottir H, Robinson JT, Mesirov JP (2012) Integrative Genomics Viewer (IGV): high-performance genomics data visualization and exploration. *Brief Bioinform* 14: 178–92. https://doi.org/10.1093/bib/bbs017 PMID: 22517427

106. Loll-Krippleber R, d'Enfert C, Feri A, Diogo D, Perin A, et al. (2014) A study of the DNA damage checkpoint in *Candida albicans*: uncoupling of the functions of Rad53 in DNA repair, cell cycle regulation and genotoxic stress-induced polarized growth. *Mol Microbiol* 91: 452–471.

107. Walther A, Wendland J (2003) An improved transformation protocol for the human fungal pathogen *Candida albicans*. *Curr Genet* 42: 339–343.
108. Yu JH, Hamari Z, Han KH, Seo JA, Reyes-Dominguez Y, et al. (2004) Double-joint PCR: a PCR-based molecular tool for gene manipulations in filamentous fungi. Fungal Genet Biol 41: 973-981.
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109. Legrand M, Bachellier-Bassi S, Lee KK, Chaudhari Y, Tournu H, et al. (2018) Generating genomic platforms to study *Candida albicans* pathogenesis. Nucleic Acids Res 46: 6935-6949.

110. Basso LR Jr., Bartiss A, Mao Y, Gast CE, Coelho PS, et al. (2010) Transformation of *Candida albicans* with a synthetic hygromycin B resistance gene. Yeast 27: 1039-1048.
108. Yu JH, Hamari Z, Han KH, Seo JA, Reyes-Dominguez Y, et al. (2004) Double-joint PCR: a PCR-based molecular tool for gene manipulations in filamentous fungi. Fungal Genet Biol 41: 973–981.
https://doi.org/10.1016/j.fgb.2004.08.001 PMID: 15465386

109. Legrand M, Bachellier-Bassi S, Lee KK, Chaudhari Y, Tournu H, et al. (2018) Generating genomic platforms to study *Candida albicans* pathogenesis. Nucleic Acids Res 46: 6935–6949.

110. Basso LR Jr., Bartiss A, Mao Y, Gast CE, Coelho PS, et al. (2010) Transformation of *Candida albicans* with a synthetic hygromycin B resistance gene. Yeast 27: 1039–1048.