MIG-10 (lamellipodin) has netrin-independent functions and is a FOS-1A transcriptional target during anchor cell invasion in <i>C. elegans</i>

Wang, Zheng; Chi, Qiuyi; Sherwood, David R.

doi:10.1242/dev.102434

Cited by 23 publications

(34 citation statements)

References 78 publications

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“…We also found that two additional MMPs expressed in the AC, zmp-3 and zmp-6 , were dependent on nhr-67 (Figure 4A and 4B). Finally, we examined the expression of actin regulators that promote invasive cellular behavior (Li et al, 2014; Wang et al, 2014). We found that AC expression of the actin regulators exc-6 (formin) and unc-34 (Ena/VASP) was dependent on NHR-67 activity, as RNAi depletion of nhr-67 resulted in reduced expression of exc-6 and unc-34 GFP transcriptional reporters (Figure 4A and 4B).…”

Section: Resultsmentioning

confidence: 99%

“…AC invasion is coordinated with the underlying vulval precursor cell P6.p divisions—the AC is specified at the P6.p one-cell stage, initiates invasion at the P6.p two-cell stage and completes invasion at the P6.p four-cell stage (Sherwood and Sternberg, 2003). Prior to invasion, a number of genes are upregulated in the AC that contribute to BM breaching, including the MMP zmp-1 , actin regulators, and the extracellular matrix component hemicentin (Morrissey et al, 2014; Sherwood et al, 2005; Wang et al, 2014; Ziel et al, 2009). Further, similar to metastatic cancer cells, the AC forms invadopodia that breach the BM (Hagedorn et al, 2014; Hagedorn et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

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Invasive Cell Fate Requires G1 Cell-Cycle Arrest and Histone Deacetylase-Mediated Changes in Gene Expression

et al. 2015

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SUMMARY Despite critical roles in development and cancer, the mechanisms that specify invasive cellular behavior are poorly understood. Through a screen of transcription factors in Caenorhabditis elegans, we identified G1 cell-cycle arrest as a precisely regulated requirement of the anchor cell (AC) invasion program. We show that the nuclear receptor nhr-67/tlx directs the AC into G1 arrest in part through regulation of the cyclin-dependent kinase inhibitor cki-1. Loss of nhr-67 resulted in non-invasive, mitotic ACs that failed to express matrix metalloproteinases or actin regulators and lack invadopodia—F-actin rich membrane protrusions that facilitate invasion. We further show that G1 arrest is necessary for the histone deacetylase HDA-1, a key regulator of differentiation, to promote pro-invasive gene expression and invadopodia formation. Together these results suggest that invasive cell fate requires G1 arrest and that strategies targeting both G1 arrested and actively cycling cells may be needed to halt metastatic cancer.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Invasive Cell Fate Requires G1 Cell-Cycle Arrest and Histone Deacetylase-Mediated Changes in Gene Expression

et al. 2015

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“…et al 2013; Ghosh and Sternberg 2014;Wang et al 2014b). The contactin RIG-6 also functions cell autonomously in the canal, potentially as part of the UNC-53 pathway (Katidou et al 2013).…”

Section: Cytoskeletal Organization In the Growing Canalsmentioning

confidence: 99%

The Caenorhabditis elegans Excretory System: A Model for Tubulogenesis, Cell Fate Specification, and Plasticity

Sundaram

Buechner

2016

Genetics

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The excretory system of the nematode Caenorhabditis elegans is a superb model of tubular organogenesis involving a minimum of cells. The system consists of just three unicellular tubes (canal, duct, and pore), a secretory gland, and two associated neurons. Just as in more complex organs, cells of the excretory system must first adopt specific identities and then coordinate diverse processes to form tubes of appropriate topology, shape, connectivity, and physiological function. The unicellular topology of excretory tubes, their varied and sometimes complex shapes, and the dynamic reprogramming of cell identity and remodeling of tube connectivity that occur during larval development are particularly fascinating features of this organ. The physiological roles of the excretory system in osmoregulation and other aspects of the animal's life cycle are only beginning to be explored. The cellular mechanisms and molecular pathways used to build and shape excretory tubes appear similar to those used in both unicellular and multicellular tubes in more complex organs, such as the vertebrate vascular system and kidney, making this simple organ system a useful model for understanding disease processes.KEYWORDS Caenorhabditis elegans; tubulogenesis; excretory-secretory system; WormBook

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“…During AC invasion, the c-fos transcription factor ortholog fos-1 promotes expression the zinc metalloprotease zmp-1, the protocadherin cdh-3, the zinc finger protein egl-43, the hemicentin extracellular matrix protein gene him-4, and lamillopodin/mig-10; the activities of these genes induce the AC to form ventrally directed protrusions that breach the basement membrane ( Fig. 6A; Sherwood et al, 2005;Hwang et al 2007;Wang et al, 2014). RNAi against the AC invasion genes resulted in defects in utse development (Table 2E; Fig.…”

Section: Ac Invasion Genes Act During L4 To Affect Utse Developmentmentioning

confidence: 99%

“…Each of these genes are expressed within the AC during invasion (Sherwood et al, 2005;Hwang et al 2007;Wang et al, 2014). Since the AC nucleus is necessary for utse development, we asked if these genes were transcriptionally active throughout L4 and were present in the utse.…”

Section: Ac Invasion Genes Act During L4 To Affect Utse Developmentmentioning

confidence: 99%

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

Ghosh

Sternberg

2014

Developmental Biology

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The Caenorhabditis elegans uterine seam cell (utse) is an H-shaped syncytium that connects the uterus to the body wall. Comprising nine nuclei that move outward in a bidirectional manner, this synctium undergoes remarkable shape change during development. Using cell ablation experiments, we show that three surrounding cell types affect utse development: the uterine toroids, the anchor cell and the sex myoblasts. The presence of the anchor cell (AC) nucleus within the utse is necessary for proper utse development and AC invasion genes fos-1, cdh-3, him-4, egl-43, zmp-1 and mig-10 promote utse cell outgrowth. Two types of uterine lumen epithelial cells, uterine toroid 1 (ut1) and uterine toroid 2 (ut2), mediate proper utse outgrowth and we show roles in utse development for two genes expressed in the uterine toroids: the RASEF ortholog rsef-1 and Trio/unc-73. The SM expressed gene unc-53/NAV regulates utse cell shape; ablation of sex myoblasts (SMs), which generate uterine and vulval muscles, cause defects in utse morphology. Our results clarify the nature of the interactions that exist between utse and surrounding tissue, identify new roles for genes involved in cell outgrowth, and present the utse as a new model system for understanding cell shape change and, putatively, diseases associated with cell shape change.

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MIG-10 (lamellipodin) has netrin-independent functions and is a FOS-1A transcriptional target during anchor cell invasion in C. elegans

Cited by 23 publications

References 78 publications

Invasive Cell Fate Requires G1 Cell-Cycle Arrest and Histone Deacetylase-Mediated Changes in Gene Expression

Invasive Cell Fate Requires G1 Cell-Cycle Arrest and Histone Deacetylase-Mediated Changes in Gene Expression

The Caenorhabditis elegans Excretory System: A Model for Tubulogenesis, Cell Fate Specification, and Plasticity

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

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