## 3 Discussion  
Microtubules are evolutionarily conserved principal components of the cytoskeleton across eukaryotic cells. Tubulins tightly regulate structural dynamics and polymerization, define the polymerization of microtubules, and constitute the central building blocks of  
Figure 6: PcTbcc1 is essential for the full virulence of _P. capsaicin_. (**a**) Virulence characteristics of the wild-type, \(\Delta\)_Pcthcc1-212_, \(\Delta\)_Pcthcc1-297_, _Pcthcc1-72A115-611_, _Pcthcc1-124A115-611_, and EV strains against 4-week-old _P. capsaicin_-susceptibleHNUCB0226 bell pepper seedlings at 72 hpi. (**b**) Statistical computation of disease severity index through the quantification and scoring of the different types of blight lesions on leaf tissues of pepper seedlings independently inoculated with individual strains after 72 hpi. Consistent results from five independent biological experiments, each with three technical replicates, were used for statistical analyses. Statistical significance was analyzed using a one-way ANOVA (non-parametric) approach. In each biological experiment, we inoculated 20 seedlings per strain. Therefore, the total number of seedlings (n) per strain is n = 20 \(\times\) 5.  
microtubules [16]. Microtubules play indispensable regulatory roles in vital cellular processes, including mitotic cell division, cell motility, the progression of cellular transport, pathogenesis, and the maintenance of cell structure and shape [17; 18]. Microtubule dysfunction has been linked to several life-threatening diseases, including Alzheimer's disease, hearing impairment, and cancer [19]. In the current study, transcriptomic investigations revealed significant upregulation in the expression pattern of the single-copy _P. capsici_ gene _PcTBCC1_, which codes for a hypothetical protein containing the tubulin-binding cofactor C (TBCC) domain during pathogen-host interactions, indicating the potential contribution of _PcTBCC-1_ to the pathogenesis of the Phytophthora blight pathogen. We demonstrated that TBCC sequences obtained from sixteen organisms possess the conserved TBCC domain and that the novel TBCC domain-containing protein identified in _P. capsici_ shares closer evolutionary ties with _Aureococcus anophageferens_ (an alga pelagophyte that causes harmful brown tide blooms in marine embayments) [20], and two economic pathogenic oomycetes, _Phyophthora infestans_ and _Saprolegnia parasitica_[21; 22], but is evolutionarily distant from the phytopathogenic oomycetes _Phyophthora sojae_ and selected fungi and plants. Based on these observations, we speculated that PcTBcc1 affects the infection characteristics of _P. capsici_ by regulating unique infection-related pathways that may have been lost in some pathogenic oomycetes and fungal species due to speciation. Detailed sequence feature examinations revealed Pctbcc1 as a putative non-classically secreted extracellular protein with a chloroplast-targeting peptide (cTP) signal embedded within the TBCC domain. Thus, its secretion, the precise influence of cTP on the virulence of _P. capsici_ during host-pathogen interaction, its probable roles as an effector protein, and its likely interacting partners will be the focus of subsequent investigations. T tubulin-folding cofactors (including TBCA, TBCB, TBCC, TBCD, and TBCE) accelerate morphological development in plants, animals, and fungi. For instance, in _Fusarium assiticum_, the targeted disruption of _FatTBCA_ triggers a significant reduction in vegetative growth [23]. Additionally, the TBC-mediated regulation of cell division promotes morphological development in _Zea mays_ and _Arabidopsis thaliana_[24; 25; 26]. In contrast, the targeted replacement of _PcTBCC1_ in _P. capsici_ had no adverse effects on the vegetative development of the polycyclic Phytophthora hight pathogen. From these results, we hypothesized that, unlike its counterparts in plants and fungi, the regulatory roles of PcTbcc1 in _P. capsici_ likely overlap with those of other members of the tubulin-folding cofactor family.