Spatial and molecular cues for cell outgrowth during C. elegans uterine development

Ghosh, Srimoyee; Sternberg, Paul W.

doi:10.1016/j.ydbio.2014.09.028

Cited by 26 publications

(22 citation statements)

References 102 publications

(101 reference statements)

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“…However, loss of lin-29 does not cause any detectable abnormality in Sp-Ut valve core morphology ( Fig 5A). Moreover, it has been reported that anchor cell invasion genes (fos-1, mig-10, egl-43, cdh-3, and zmp-1) are involved in utse development (Ghosh and Sternberg, 2014), but we did not observe any abnormality in the Sp-Ut valve upon RNAi knockdown of these genes (data not shown). Nevertheless, it will be interesting to examine whether the physical connection between the hypodermal seam and gonadal utse is formed properly in lin-28(lf) hermaphrodites.…”

Section: Discussionmentioning

confidence: 48%

“…The utse connects the uterus to the seam cells laterally and also to uv1 and vulva cells. egl-13:GFP is expressed in the nuclei of π cell lineage, whose products includes the utse, from late L3 to L4 stages (Ghosh and Sternberg, 2014). Utse labeled by egl-13:GFP migrated laterally in wild-type hermaphrodites (Fig S4A,B).…”

Section: Sp-ut Valve Morphogenesis Uterus Lumen Formation and Utse mentioning

confidence: 99%

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TheC. elegansheterochronic genelin-28coordinates the timing of hypodermal and somatic gonadal programs for hermaphrodite reproductive system morphogenesis

Choi

Ambros

2018

Preprint

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C. elegans heterochronic genes determine the timing of expression of specific cell fates in particular stages of developing larva. However, their broader roles in coordinating developmental events across diverse tissues has been less well investigated. Here, we show that loss of lin-28, a central heterochronic regulator of hypodermal development, causes reduced fertility associated with abnormal somatic gonad morphology.In particular, the abnormal spermatheca-uterine valve morphology of lin-28(lf) hermaphrodites trap embryos in the spermatheca, which disrupts ovulation and causes embryonic lethality. The same genes that act downstream of lin-28 in the regulation of hypodermal developmental timing also act downstream of lin-28 in somatic gonad morphogenesis and fertility. Importantly, we find that hypodermal expression, but not somatic gonadal expression, of lin-28 is sufficient for restoring normal somatic gonad morphology in lin-28(lf) mutants. We propose that the abnormal somatic gonad morphogenesis of lin-28(lf) hermaphrodites results from temporal discoordination between the accelerated hypodermal development and normally timed somatic gonad development. Thus, our findings exemplify how a cell-intrinsic developmental timing program can also control cell non-autonomous signaling critical for proper development of other interacting tissues.

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Section: Discussionmentioning

confidence: 48%

Section: Sp-ut Valve Morphogenesis Uterus Lumen Formation and Utse mentioning

confidence: 99%

TheC. elegansheterochronic genelin-28coordinates the timing of hypodermal and somatic gonadal programs for hermaphrodite reproductive system morphogenesis

Choi

Ambros

2018

Preprint

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“…The utse connects the uterus to the seam cells laterally and also to uv1 and the vulva. egl-13p::GFP is expressed in the nuclei of π cell lineage, the products of which include the utse cells, from late L3 to L4 stages (Ghosh and Sternberg, 2014). Utse cells labeled by egl-13p::GFP migrated laterally in wild-type hermaphrodites (Fig.…”

Section: Defects In Ovulation and Spermathecal Exit Cause Reduced Embmentioning

confidence: 98%

The C. elegans heterochronic gene lin-28 coordinates the timing of hypodermal and somatic gonadal programs for hermaphrodite reproductive system morphogenesis

Choi

Ambros

2019

Development

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C. elegans heterochronic genes determine the timing of expression of specific cell fates in particular stages of developing larvae. However, their broader roles in coordinating developmental events across diverse tissues have been less well investigated. Here, we show that loss of lin-28, a central heterochronic regulator of hypodermal development, causes reduced fertility associated with abnormal somatic gonadal morphology. In particular, the abnormal spermatheca-uterine valve morphology of lin-28(lf) hermaphrodites traps embryos in the spermatheca, which disrupts ovulation and causes embryonic lethality. The same genes that act downstream of lin-28 in the regulation of hypodermal developmental timing also act downstream of lin-28 in somatic gonadal morphogenesis and fertility. Importantly, we find that hypodermal expression, but not somatic gonadal expression, of lin-28 is sufficient for restoring normal somatic gonadal morphology in lin-28(lf) mutants. We propose that the abnormal somatic gonadal morphogenesis of lin-28(lf) hermaphrodites results from temporal discoordination between the accelerated hypodermal development and normally timed somatic gonadal development. Thus, our findings exemplify how a cell-intrinsic developmental timing program can also control proper development of other interacting tissues, presumably by cell non-autonomous signal(s). This article has an associated 'The people behind the papers' interview.

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“…The uterus itself comprises the ut1-ut4 uterine toroid cells and du cells that together form a tube to hold eggs. Eggs pass from the uterus into the vulva through a junction comprising the uterine seam (utse) and uterine-ventral (uv1 and uv3) cells, and the vulva itself comprises several types of vulval toroid (vt) cells (Schindler and Sherwood, 2014;Ghosh and Sternberg, 2014;Ecsedi et al, 2015).…”

Section: Cells Of the Egg-laying Systemmentioning

confidence: 99%

Cellular expression and functional roles of all 26 neurotransmitter GPCRs in theC. elegansegg-laying circuit

Fernandez

Wei

Wang

et al. 2020

Preprint

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Maps of the synapses made and neurotransmitters released by all neurons in model systems such as C. elegans have left still unresolved how neural circuits integrate and respond to neurotransmitter signals. Using the egg-laying circuit of C. elegans as a model, we mapped which cells express each of the 26 neurotransmitter G protein coupled receptors (GPCRs) of this organism and also genetically analyzed the functions of all 26 GPCRs. We found that individual neurons express many distinct receptors, epithelial cells often express neurotransmitter receptors, and receptors are often positioned to receive extrasynaptic signals. The egg-laying circuit appears to use redundancy and compensation to achieve functional robustness, as receptor knockouts reveal few defects; however, increasing receptor signaling through overexpression more efficiently reveals receptor functions. This map of neurotransmitter GPCR expression and function in the egg-laying circuit provides a model for understanding GPCR signaling in other neural circuits.

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Spatial and molecular cues for cell outgrowth during C. elegans uterine development

Cited by 26 publications

References 102 publications

TheC. elegansheterochronic genelin-28coordinates the timing of hypodermal and somatic gonadal programs for hermaphrodite reproductive system morphogenesis

TheC. elegansheterochronic genelin-28coordinates the timing of hypodermal and somatic gonadal programs for hermaphrodite reproductive system morphogenesis

The C. elegans heterochronic gene lin-28 coordinates the timing of hypodermal and somatic gonadal programs for hermaphrodite reproductive system morphogenesis

Cellular expression and functional roles of all 26 neurotransmitter GPCRs in theC. elegansegg-laying circuit

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