bluuebunny/crossref_metadata_2025_split huggingface dataset:
Genes of the Enhancer of split and achaete-scute complexes are required for a regulatory loop between Notch and Delta during lateral signalling in Drosophila
Authors: Heitzler Pascal , Bourouis Marc , Ruel Laurent , Carteret Cathie , Simpson Pat 
Published: April 2021

ABSTRACT
Like the neuroblasts of the central nervous system, sensory organ precursors of the peripheral nervous system of the Drosophila thorax arise as single spaced cells. However, groups of cells initially have neural potential as visualized by the expression of the proneural genes achaete and scute. A class of genes, known as the ‘neurogenic genes’, function to restrict the proportion of cells that differentiate as sensory organ precursors. They mediate cell communication between the competent cells by means of an inhibitory signal, Delta, that is transduced through the Notch receptor and results in a cessation of achaete-scute activity. Here we show that mutation of either the bHLH-encoding genes of the Enhancer of split complex (E(spl)-C) or groucho, like Notch or Delta mutants, cause an overproduction of sensory organ precursors at the expense of epidermis. The mutant cells behave autonomously suggesting that the corresponding gene products are required for reception of the inhibitory signal. Epistasis experiments place both E(spl)-C bHLH-encoding genes and groucho downstream of Notch and upstream of achaete and scute, consistent with the idea that they are part of the Notch signalling cascade. Since all competent cells produce both the receptor and its ligand, it was postulated that Notch and Delta are linked within each cell by a feedback loop. We show, that, like mutant Notch cells, cells mutant for E(spl)-C bHLH-encoding genes or groucho inhibit neighbouring wild-type cells causing them to adopt the epidermal fate. This inhibition requires the genes of the achaete-scute complex (AS-C) which must therefore regulate the signal Delta. Thus there is a regulatory loop between Notch and Delta that is under the transcriptional control of the E(spl)-C and AS-C genes.
Pax1 is expressed during development of the thymus epithelium and is required for normal T-cell maturation
Authors: Wallin Johan , Eibel Hermann , Neubüser Annette , Wilting Jörg , Koseki Haruhiko , Balling Rudi 
Published: April 2021

ABSTRACT
Pax1 is a transcriptional regulatory protein expressed during mouse embryogenesis and has been shown to have an important function in vertebral column development. Expression of Pax1 mRNA in the embryonic thymus has been reported previously. Here we show that Pax1 protein expression in thymic epithelial cells can be detected throughout thymic development and in the adult. Expression starts in the early endodermal epithelium lining the foregut region and includes the epithelium of the third pharyngeal pouch, a structure giving rise to part of the thymus epithelium. In early stages of thymus development a large proportion of thymus cells expresses Pax1. With increasing age, the proportion of Pax1-expressing cells is reduced and in the adult mouse only a small fraction of cortical thymic stromal cells retains strong Pax1 expression. Expression of Pax1 in thymus epithelium is necessary for establishing the thymus microenvironment required for normal T cell maturation. Mutations in the Pax-1 gene in undulated mice affect not only the total size of the thymus but also the maturation of thymocytes. The number of thymocytes is reduced about 2- to 5-fold, affecting mainly the CD4+8+ immature and CD4+ mature thymocyte subsets. The expression levels of major thymocyte surface markers remains unchanged with the exception of Thy-1 which was found to be expressed at 3- to 4-fold higher levels.
encore, a gene required for the regulation of germ line mitosis and oocyte differentiation during Drosophila oogenesis
Authors: Hawkins Nancy C. , Thorpe Julie , Schüpbach Trudi 
Published: April 2021

ABSTRACT
During Drosophila oogenesis, a stem cell daughter undergoes precisely four rounds of mitosis to generate a cyst of 16 cells interconnected by cytoplasmic bridges. One of the cells becomes the oocyte while the remaining 15 cells differentiate as nurse cells. We have identified a gene, encore, that is involved both in regulating the number of germline mitoses and in the process of oocyte differentation. Mutations in encore result in exactly one extra round of mitosis in the germline. Genetic and molecular studies indicate that this mitotic defect may be mediated through the gene bag-of-marbles. The isolation and characterization of mutiple alleles of encore revealed that they were all temperature sensitive for this phentoype. Mutations in encore also affect the process of oocyte differentiation. Egg chambers are produced in which the oocyte nucleus has undergone endoreplication often resulting in the formation of 16 nurse cells. We argue that these two phenotypes produced by mutations in encore represent two independent requirements for encore during oogenesis.
Activation and function of Notch at the dorsal-ventral boundary of the wing imaginal disc
Authors: Celis Jose F. de , Garcia-Bellido Antonio , Bray Sarah J. 
Published: April 2021

ABSTRACT
The cells along the dorsoventral boundary of the Drosophila wing imaginal disc have distinctive properties and their specification requires Notch activity. Later in development, these cells will form the wing margin, where sensory organs and specialised trichomes appear in a char-acteristic pattern. We find that Notch is locally activated in these cells, as demonstrated by the restricted expression of the Enhancer of split proteins in dorsal and ventral cells abutting the D/V boundary throughout the third larval instar. Furthermore other genes identified by their involve-ment in Notch signaling during neurogenesis, such as Delta and Suppressor of Hairless, also participate in Notch function at the dorsoventral boundary. In addition, Serrate, a similar transmembrane protein to Delta, behaves as a ligand required in dorsal cells to activate Notch at the boundary. Notch gain-of-function alleles in which Notch activity is not restricted to the dorsoventral boundary cause miss-expression of cut and wingless and overgrowth of the disc, illustrating the importance of localised Notch activa-tion for wing development.
The WUSCHEL gene is required for shoot and floral meristem integrity in Arabidopsis
Authors: Laux Thomas , Mayer Klaus F. X. , Berger Jürgen , Jürgens Gerd 
Published: April 2021

ABSTRACT
Self perpetuation of the shoot meristem is essential for the repetitive initiation of shoot structures during plant devel-opment. In Arabidopsis shoot meristem maintenance is disrupted by recessive mutations in the WUSCHEL (WUS) gene. The defect is evident at all developmental stages and is restricted to shoot and floral meristems, whereas the root meristem is not affected. wus mutants fail to properly organize a shoot meristem in the embryo. Postembryoni-cally, defective shoot meristems are initiated repetitively but terminate prematurely in aberrant flat structures. In contrast to wild-type shoot meristems, primordia initiation occurs ectopically across mutant apices, including the center, and often new shoot meristems instead of organs are initiated. The cells of wus shoot apices are larger and more vacuolated than wild-type shoot meristem cells. wus floral meristems terminate prematurely in a central stamen. Double mutant studies indicate that the number of organ primordia in the center of wus flowers is limited, irrespective of organ identity and we propose that meristem cells are allocated into floral whorl domains in a sequential manner. WUS activity also appears to be required for the formation of supernumerary organs in the center of agamous, superman or clavata1 flowers, suggest-ing that the WUS gene acts upstream of the corresponding genes. Our results suggest that the WUS gene is specifically required for central meristem identity of shoot and floral meristems to maintain their structural and functional integrity.
Spatial and temporal patterns of c-kit-expressing cells in WlacZ/+ and WlacZ/WlacZ mouse embryos
Authors: Bernex Florence , Sepulveda Paulo De , Kress Chantal , Elbaz Colette , Delouis Claude , Panthier Jean-Jacques 
Published: April 2021

ABSTRACT
In the mouse, the Kit receptor and its ligand, the stem cell factor (SCF), are encoded at the W/Kit and Steel loci, respectively. The Kit/SCF transduction pathway is involved in promoting cellular migration, proliferation and/or survival of melanoblasts, hematopoietic progenitors and primordial germ cells. Furthermore, a functional Kit/SCF pathway is required for the development of interstitial cells of Cajal (ICC) in the small intestine. Whereas all c-kit-expressing cells in embryogenesis were not identified, previous studies clearly demonstrated that the c-kit expression pattern extends well beyond cells known to be affected by W mutations. To investigate further Kit function, we specifically marked the c-kit-expressing cells and followed their fate during embryogenesis. A mutation was introduced by gene targeting at the W/Kit locus in mouse embryonic stem cells. The lacZ reporter gene was inserted into the first exon of c-kit, thus creating a null allele, called WlacZ.
The lacZ expression reflects normal expression of the c-kit gene in WlacZ/+ embryos. The comparison of the patterns of lacZ-expressing cells between WlacZ/+ and WlacZ/WlacZ embryos allowed us to detect where and when melanoblasts, primordial germ cells and hematopoietic progenitors failed to survive in the absence of Kit. We also observed that ICC express c-kit during embryogenesis. ICC are found identically in WlacZ/+ and WlacZ/WlacZ embryos. Therefore, ICC do not depend on Kit expression during embryogenesis. These results indicate that the function of the c-kit gene is only required for the postnatal development of the ICC.
Unexpected sites of c-kit expression were uncovered in embryos, including endothelial, epithelial and endocrine cells. None of these cells are dependent on Kit expression for their migration, proliferation and/or survival during embryogenesis. Nevertheless, we assume that the Kit/SCF pathway could be involved in the growth of transformed endothelial, epithelial and endocrine cells.
The Drosophila embryonic midline is the site of Spitz processing, and induces activation of the EGF receptor in the ventral ectoderm
Authors: Golembo Myriam , Raz Erez , Shilo Ben-Zion 
Published: April 2021

ABSTRACT
The Drosophila EGF receptor (DER) is activated by secreted Spitz to induce different cell fates in the ventral ectoderm. Processing of the precursor transmembrane Spitz to generate the secreted form was shown to be the limiting event, but the cells in which processing takes place and the mechanism that may generate a gradient of secreted Spitz in the ectoderm were not known. The ectodermal defects in single minded (sim) mutant embryos, in which the midline fails to develop, suggested that the midline cells contribute to patterning of the ventral ectoderm. This work shows that the midline provides the site for Spitz expression and processing. The Rhomboid and Star proteins are also expressed and required in the midline. The ectodermal defects of spitz, rho or Star mutant embryos could be rescued by inducing the expression of the respective normal genes only in the midline cells. Rho and Star thus function non-autonomously, and may be required for the production or processing of the Spitz precursor. Secreted Spitz is the only sim-dependent contribution of the midline to patterning the ectoderm, since the ventral defects observed in sim mutant embryos can be overcome by expression of secreted Spitz in the ectoderm. While ectopic expression of secreted Spitz in the ectoderm or mesoderm gave rise to ventralization of the embryo, increased expression of secreted Spitz in the midline did not lead to alterations in ectoderm patterning. A mechanism for adjustment to variable levels of secreted Spitz emanating from the midline may be provided by Argos, which forms an inhibitory feedback loop for DER activation. The production of secreted Spitz in the midline, may provide a stable source for graded DER activation in the ventral ectoderm.
A posteriorising factor, retinoic acid, reveals that anteroposterior patterning controls the timing of neuronal differentiation in Xenopus neuroectoderm
Authors: Papalopulu Nancy , Kintner Chris 
Published: April 2021

ABSTRACT
During early development of the Xenopus central nervous system (CNS), neuronal differentiation can be detected posteriorly at neural plate stages but is delayed anteriorly until after neural tube closure. A similar delay in neuronal differentiation also occurs in the anterior neural tissue that forms in vitro when isolated ectoderm is treated with the neural inducer noggin. Here we examine the factors that control the timing of neuronal differentiation both in embryos and in neural tissue induced by noggin (noggin caps). We show that the delay in neuronal differentiation that occurs in noggin caps cannot be overcome by inhibiting the activity of the neurogenic gene, X-Delta-1, which normally inhibits neuronal differentiation, suggesting that it represents a novel level of regulation. Conversely, we show that the timing of neuronal differentiation can be changed from late to early after treating noggin caps or embryos with retinoic acid (RA), a putative posteriorising agent. Concommittal with changes in the timing of neuronal differentiation, RA suppresses the expression of anterior neural genes and promotes the expression of posterior neural genes. The level of early neuronal differentiation induced by RA alone is greatly increased by the additional expression of the proneural gene, XASH3. These results indicate that early neuronal differentiation in neuralised ectoderm requires posteriorising signals, as well as signals that promote the activity of proneural genes such as XASH3. In addition, these result suggest that neuronal differentiation is controlled by anteroposterior (A-P) patterning, which exerts a temporal control on the onset of neuronal differentiation.
Non-cell-autonomous function of the Antirrhinum floral homeotic proteins DEFICIENS and GLOBOSA is exerted by their polar cell-to-cell trafficking
Authors: Perbal Marie-Christine , Haughn George , Saedler Heinz , Schwarz-Sommer Zsuzsanna 
Published: April 2021

ABSTRACT
In Antirrhinum majus, petal and stamen organ identity is controlled by two MADS-box transcription factors, DEFICIENS and GLOBOSA. Mutations in either of these genes result in the replacement of petals by sepaloid organs and stamens by carpelloid organs. Somatically stable def and glo periclinal chimeras, generated by transposon excision events, were used to study the non-cell-autonomous functions of these two MADS-box proteins. Two morphologically distinct types of chimeras were analysed using genetic, morphological and molecular techniques. Restoration of DEF expression in the L1 cell layer results in the reestablishment of DEF and GLO functions in L1-derived cells only; inner layer cells retain their mutant sepaloid features. Nevertheless, this activity is sufficient to allow the expansion of petal lobes, highlighting the role of DEF in the stimulation of cell proliferation and/or cell shape and elongation when expressed in the L1 layer. Establishment of DEF or GLO expression in L2 and L3 cell layers is accompanied by the recovery of petaloid identity of the epidermal cells but it is insufficient to allow petal lobe expansion. We show by in situ immunolocalisation that the non-cell-autonomy is due to direct trafficking of DEF and GLO proteins from the inner layer to the epidermal cells. At least for DEF, this movement appears to be polar since DEF acts cell-autonomously when expressed in the L1 cell layer. Furthermore, the petaloid revertant sectors observed on second whorl mutant organs and the mutant margins of petals of L2L3 chimeras suggest that DEF and GLO intradermal movement is limited. This restriction may reflect the difference in the regulation of primary plasmodesmata connecting cells from the same layer and secondary plasmodesmata connecting cells from different layers. We propose that control of intradermal trafficking of DEF and GLO could play a role in maintaining of the boundaries of their expression domains.
A proteoglycan that activates fibroblast growth factors during early neuronal development is a perlecan variant
Authors: Joseph Sharon J. , Ford Miriam D. , Barth Christian , Portbury Stuart , Bartlett Perry F. , Nurcombe Victor , Greferath Ursula 
Published: April 2021

ABSTRACT
Cells in the early embryonic vertebrate nervous system are dependent on members of the fibroblast growth factor (FGF) family for their proliferation and subsequent differentiation. These growth factors will only bind to their specific high affinity cell surface receptors after formation of a ternary complex with the glycosaminoglycan heparan sulfate. Such specific heparan sulfates are secreted as proteoglycans from neural precursor cells and localise to their surfaces. One such proteoglycan, HSPG-PRM (Perlecanrelated molecule), was isolated through its ability to potentiate neural cell responses to either FGF-1 or FGF-2. In this study, we have verified the relative molecular mass of the core protein of PRM as 45,000 and obtained partial amino acid sequence from it. The sequences bore significant homology to native perlecan. A probe generated by reverse transcriptase polymerase chain reaction using oligonucleotides designed from the protein sequence used on northern blots of RNA from a neuroepithelial cell line detected perlecan at 12.6 kilobases, as well as novel transcripts at 6.5 and 3.5 kilobases. The latter species appears by virtue of its size and abundance to be the novel PRM transcript. PRM appears to be encoded by the same gene as perlecan, as genomic Southern blotting only detected a single gene. Polyclonal antibodies raised against the PRM molecule detected a single proteoglycan species at 290×103 with a core protein of 45×103. Polyclonal anti-perlecan antibodies cross-reacted with PRM confirming their relatedness, although immunohistochemical studies revealed a differential staining pattern for PRM as compared to perlecan within the developing nervous system. The PRM molecule was shown to be localised to several different tissues of the developing embryo, indicating that it plays a broad role. We conclude that PRM is a variant of perlecan that is differentially glycosylated in a manner that confers highly specific functions at critical stages of neural development and tissue growth.
Asymmetric distribution of the C. elegans HAM-1 protein in neuroblasts enables daughter cells to adopt distinct fates
Authors: Guenther Catherine , Garriga Gian 
Published: April 2021

ABSTRACT
One mechanism of generating cellular diversity is to distribute developmental potential asymmetrically to daughter cells at mitosis. Two observations described in this report suggest that the C. elegans HAM-1 protein functions in dividing neuroblasts to produce daughter cells that adopt distinct fates. First, HAM-1 is asymmetrically distributed to the periphery of certain mitotic cells, ensuring that it will be inherited by only one daughter cell. Second, ham-1 mutations disrupt the asymmetric divisions of five neuroblasts. In one of these divisions, loss of ham-1 function causes the daughter cell that does not inherit HAM-1 to adopt the fate of the daughter cell that normally inherits HAM-1. We propose that asymmetric distribution of HAM-1 enables daughter cells to adopt distinct fates.
Drosophila brachyenteron regulates gene activity and morphogenesis in the gut
Authors: Singer Jonathan B. , Harbecke Ruth , Kusch Thomas , Reuter Rolf , Lengyel Judith A. 
Published: April 2021

ABSTRACT
Chromosomal region 68D/E is required for various aspects of Drosophila gut development; within this region maps the Brachyury homolog T-related gene (Trg), DNA of which rescues the hindgut defects of deficiency 68D/E. From a screen of 13,000 mutagenized chromosomes we identified six non-complementing alleles that are lethal over deficiencies of 68D/E and show a hindgut phenotype. These mutations constitute an allelic series and are all rescued to viability by a Trg transgene. We have named the mutant alleles and the genetic locus they define brachyenteron (byn); phenotypic characterization of the strongest alleles allows determination of the role of byn in embryogenesis. byn expression is activated by tailless, but byn does not regulate itself. byn expression in the hindgut and anal pad primordia is required for the regulation of genes encoding transcription factors (even-skipped, engrailed, caudal, AbdominalB and orthopedia) and cell signaling molecules (wingless and decapentaplegic). In byn mutant embryos, the defective program of gene activity in these primordia is followed by apoptosis (initiated by reaper expression and completed by macrophage engulfment), resulting in severely reduced hindgut and anal pads. Although byn is not expressed in the midgut or the Malpighian tubules, it is required for the formation of midgut constrictions and for the elongation of the Malpighian tubules.
An indelible lineage marker for Xenopus using a mutated green fluorescent protein
Authors: Zernicka-Goetz M. , Pines J. , Ryan K. , Siemering K. R. , Haseloff J. , Evans M. J. , Gurdon J. B. 
Published: April 2021

ABSTRACT
We describe the use of a DNA construct (named GFP.RN3) encoding green fluorescent protein as a lineage marker for Xenopus embryos. This offers the following advantages over other lineage markers so far used in Xenopus. When injected as synthetic mRNA, its protein emits intense fluorescence in living embryos. It is non-toxic, and the fluorescence does not bleach when viewed under 480 nm light. It is surprisingly stable, being strongly visible up to the feeding tadpole stage (5 days), and in some tissues for several weeks after mRNA injection. We also describe a construct that encodes a blue fluorescent protein. We exemplify the use of this GFP.RN3 construct for marking the lineage of individual blastomeres at the 32-to 64-cell stage, and as a marker for single transplanted blastula cells. Both procedures have revealed that the descendants of one embryonic cell can contribute single muscle cells to nearly all segmental myotomes rather than predominantly to any one myotome. An independent aim of our work has been to follow the fate of cells in which an early regulatory gene has been temporarily overexpressed. For this purpose, we co-injected GFP.RN3 mRNA and mRNA for the early Xenopus gene Eomes, and found that a high concentration of Eomes results in ectopic muscle gene activation in only the injected cells. This marker may therefore be of general value in providing long term identification of those cells in which an early gene with ephemeral expression has been overexpressed.