Gene expression markers for Caenorhabditis elegans vulval cells

Inoué, Takao; Sherwood, David R.; Aspöck, Gudrun; Butler, James A.; Gupta, Bhagwati P.; Kirouac, Martha; Wang, Minqin; Lee, Pei-Yun; Kramer, James M.; Hope, Ian A.; Bürglin, Thomas R.; Sternberg, Paul W.

doi:10.1016/s0925-4773(03)00117-5

Cited by 78 publications

(88 citation statements)

References 24 publications

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“…1E, Tables 1 and 2, and Fig. 5, which is published as supporting information on the PNAS web site) (9). By contrast, lin-29 in not required for the expression of cdh-3 in vulC, vulD, vulE, vulF (9), ceh-2 in vulB (9), egl-17 in vulE and vulF (23), and zmp-1 in vulA (9).…”

Section: Resultsmentioning

confidence: 96%

“…1B). Previously described genes of this type include cdh-3 (14), egl-17 (15), lin-3 (16), zmp-1 (9,17), ceh-2 (9), T04B2.6 (9), F47B8.6 (9), B0034.1 (9), unc-53 (18), egl-26 (11), sqv-4 (19), bam-2 (20), and syg-2 (21). egl-26 was previously reported to express in vulE and vulB2 cells (11).…”

Section: Resultsmentioning

confidence: 99%

“…For example, cdh-3 is expressed in early L4, F47B8.6 is expressed in late L4, and T04B2.6 is expressed Ϸ1 day after the L4-to-adult molt (9). For egl-17, ceh-2, zmp-1, and sqv-4, the timing of gene expression is different for different vulval cells (9,15,19). For example, egl-17 is expressed in vulE and vulF cells in the L3 stage and in vulC and vulD in the L4 stage.…”

Section: Resultsmentioning

confidence: 99%

“…5, which is published as supporting information on the PNAS web site) (9). By contrast, lin-29 in not required for the expression of cdh-3 in vulC, vulD, vulE, vulF (9), ceh-2 in vulB (9), egl-17 in vulE and vulF (23), and zmp-1 in vulA (9). Moreover, the expression of egl-17 in vulE and vulF is observed during the L4 stage (23), suggesting that the mechanism that turns off egl-17 expression in these cells is compromised (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…1A). These nuclei are in cells of seven types (vulA, vulB1, vulB2, vulC, vulD, vulE, and vulF), as evidenced by subsequent morphogenetic movements and by the pattern of gene expression (8,9) (Fig. 1B).…”

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confidence: 99%

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Transcriptional network underlying Caenorhabditis elegans vulval development

Inoué

Wang

Ririe

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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The vulval development of Caenorhabditis elegans provides an opportunity to investigate genetic networks that control gene expression during organogenesis. During the fourth larval stage (L4), seven vulval cell types are produced, each of which executes a distinct gene expression program. We analyze how the expression of cell-type-specific genes is regulated. Ras and Wnt signaling pathways play major roles in generating the spatial pattern of cell types and regulate gene expression through a network of transcription factors. One transcription factor (lin-29) primarily controls the temporal expression pattern. Other transcription factors (lin-11, cog-1, and egl-38) act in combination to control cell-typespecific gene expression. The complexity of the network arises in part because of the dynamic nature of gene expression, in part because of the presence of seven cell types, and also because there are multiple regulatory paths for gene expression within each cell type.organogenesis ͉ signaling pathways ͉ transcription D evelopmental events are driven by spatially and temporally regulated gene expression. Understanding how complex patterns of expression are produced is therefore a critical part of deciphering mechanisms of development. In general, intercellular signaling mechanisms interact with a network of transcription factors to generate cell-type-specific patterns of gene expression. The late stage of Caenorhabditis elegans vulval development offers a useful model in which to study this process. During this period of vulval development, seven distinct cell types are produced that express unique combinations of genes. Over the last several years, a number of genes were discovered that are expressed in cell-type and stage-specific patterns in the vulva, and several transcription factors were found to regulate these genes. In this paper, we synthesize and extend our current knowledge of this genetic network.The C. elegans vulva connects the uterine lumen to the outside, allowing for passage of sperm and fertilized eggs (1). Vulval cells are generated postembryonically from precursor cells P3.p P4.p, P5.p, P6.p, P7.p, and P8.p [also called vulval precursor cells (VPC)]. During the mid-third larval (L3) stage, EGF and Notch signaling induces the middle three VPCs (P5.p, P6.p, and P7.p) to adopt vulval fates, whereas P3.p, P4.p, and P8.p fuse with the hypodermal syncytium, hyp7 (2-6).During the late-L3 to the early-L4 stage, P5.p, P6.p, and P7.p undergo two or three rounds of cell division to produce 22 nuclei (7) (Fig. 1A). These nuclei are in cells of seven types (vulA, vulB1, vulB2, vulC, vulD, vulE, and vulF), as evidenced by subsequent morphogenetic movements and by the pattern of gene expression (8, 9) (Fig. 1B). The seven cell types that are present in the adult vulva represent specializations within the general epithelial cell class. These cells exhibit cell-type general features; for example, each expresses ajm-1, a component of the apical junction that connects neighboring cells in epithelial tissues (8)....

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Section: Resultsmentioning

confidence: 96%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

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Transcriptional network underlying Caenorhabditis elegans vulval development

Inoué

Wang

Ririe

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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A pair as a minimum: The two fibroblast growth factors of the nematode Caenorhabditis elegans

Birnbaum

Popovici

Roubin

2004

Developmental Dynamics

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C. elegans Vulva Induction: An In Vivo Model to Study Epidermal Growth Factor Receptor Signaling and Trafficking

Gauthier

Rocheleau

2017

Methods in Molecular Biology

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Epidermal growth factor receptor (EGFR)-mediated activation of the canonical Ras/MAPK signaling cascade is responsible for cell proliferation and cell growth. This signaling pathway is frequently overactivated in epithelial cancers; therefore, studying regulation of this pathway is crucial not only for our fundamental understanding of cell biology but also for our ability to treat EGFR-related disease. Genetic model organisms such as Caenorhabditis elegans, a hermaphroditic nematode, played a vital role in identifying components of the EGFR/Ras/MAPK pathway and delineating their order of function, and continues to play a role in identifying novel regulators of the pathway. Polarized activation of LET-23, the C. elegans homolog of EGFR, is responsible for induction of the vulval cell fate; perturbations in this signaling pathway produce either a vulvaless or multivulva phenotype. The translucent cuticle of the nematode facilitates in vivo visualization of the receptor, revealing that localization of LET-23 EGFR is tightly regulated and linked to its function. In this chapter, we review the methods used to harness vulva development as a tool for studying EGFR signaling and trafficking in C. elegans.

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Gene expression markers for Caenorhabditis elegans vulval cells

Cited by 78 publications

References 24 publications

Transcriptional network underlying Caenorhabditis elegans vulval development

Transcriptional network underlying Caenorhabditis elegans vulval development

A pair as a minimum: The two fibroblast growth factors of the nematode Caenorhabditis elegans

C. elegans Vulva Induction: An In Vivo Model to Study Epidermal Growth Factor Receptor Signaling and Trafficking

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