Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A new class B synthetic multivulva gene, ccar-1 works through the Ras pathway to regulate vulva development

ABSTRACT: Conserved Ras and Notch cell-signaling pathways promote Caenorhabditis elegans vulval cell fates. Ras pathway activity promotes the 1º vulval fate and inhibits the 2º vulval fate, and Notch pathway activity promotes the 2º vulval fate and inhibits the 1º vulval fate. Vulval cell fates are inhibited by the parallel-acting synthetic multivulva (synMuv) genes, which are grouped into either class A or B genes. We identified a new synMuv class B gene ccar-1, that works redundantly with class A genes to regulate vulva development. ccar-1 is activated by the Notch pathway to inhibit the Ras pathway in presumptive 2º vulval cells to ensure low levels of Ras pathway activity and proper 2º vulval fate specification. Our findings indicate that ccar-1 might inhibit the Ras pathway by repressing the transcription of the Ras pathway ligand lin-3 EGF. By analogy, we suggest that CCAR-1 might act as a tumor suppressor by inhibiting the expression of growth factor signals. Our study also highlights the identification of a first gain-of-function mutation that suppresses the synMuv phenotype.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE298517 | GEO | 2025/08/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcription profiling of C. elegans with activated let-60 Ras

Project description:In Caenorhabditis elegans, let-60 Ras controls many cellular processes, such as differentiation of vulval epithelial cells, function of chemosensory neurons, and meiotic progression in the germ line. Although much is known about the let-60 Ras signaling pathway, relatively little is understood about the target genes induced by let-60 Ras signaling that carry out terminal effector functions leading to morphological change. We have used DNA microarrays to identify 708 genes that change expression in response to activated let-60 Ras.

2005-07-13 | E-SMDB-1398 | biostudies-arrayexpress

Collier1996 - Delta Notch intercellular signalling and lateral inhibition

Project description:ODE model describing how slight variations in Notch and Delta cellular concentrations, through lateral inhibition, lead to cells with different states of differentiation. Lateral inhibition is a process whereby a given cell adopting a given fate prevents its immediate neighbouring cells from doing likewise. Notch and Delta are interacting transmembrane proteins and according to this model, lateral inhibition is due to a process where the inhibited cells (where notch has been activated by Delta) loose their ability to inhibit other cells (by synthesizing Delta). This process creates a feedback loop where cells with more delta proteins on their surface inhibit their immediate neighbours and adopt a different cell fate than those neighbours.

2024-09-02 | BIOMD0000001047 | BioModels

Downstream targets of let-60 Ras in Caenorhabditis elegans

2005-07-22 | E-GEOD-2974 | biostudies-arrayexpress

A conserved YAP/Notch/REST network controls the neuroendocrine cell fate in the lungs [REST & YAP1 RNA-seq]

Project description:The Notch pathway is a conserved cell-cell communication pathway that controls cell fate decisions. Here we sought to determine how Notch pathway activation inhibits the neuroendocrine cell fate in the lungs, an archetypal process for cell fate decisions orchestrated by Notch signaling that has remained poorly understood at the molecular level. Using heterogeneity in small cell lung cancer as a model system, we uncovered a role for the transcriptional regulators REST and YAP as promoters of the neuroendocrine to non-neuroendocrine transition. We further identified the specific neuroendocrine gene programs repressed by REST downstream of Notch in this process. Importantly, we validated the importance of REST and YAP in neuroendocrine to non-neuroendocrine cell fate switches in both developmental and tissue repair processes in the lungs. Altogether, these experiments identify conserved roles for REST and YAP in Notch-driven inhibition of the neuroendocrine cell fate in embryonic lungs, adult lungs, and lung cancer.

2022-02-07 | GSE171915 | GEO

A conserved YAP/Notch/REST network controls the neuroendocrine cell fate in the lungs [Hes1 RNA-seq]

2022-02-07 | GSE171914 | GEO