Regulation of anchor cell invasion and uterine cell fates by the egl-43 Evi-1 proto-oncogene in Caenorhabditis elegans

Abstract

Cell invasion is a tightly controlled process occurring during development and tumor progression. The nematode Caenorhabditis elegans serves as a genetic model to study cell invasion during normal development. In the third larval stage, the anchor cell in the somatic gonad first induces and then invades the adjacent epidermal vulval precursor cells. The homolog of the Evi-1 oncogene, egl-43, is necessary for basement membrane destruction and anchor cell invasion. egl-43 is part of a regulatory network mediating cell invasion downstream of the fos-1 proto-oncogene. In addition, EGL-43 is required to specify the cell fates of ventral uterus cells downstream of or in parallel with LIN-12 NOTCH. Comparison with mammalian Evi-1 suggests a conserved pathway controlling cell invasion and cell fate specification.

Caenorhabditis elegans FOS-1 and JUN-1 Regulateplc-1Expression in the Spermatheca to Control Ovulation

“…However, the role of AP-1 proteins in the reproductive system remains largely unexplored, due to the lack of appropriate model systems. Our findings that FOS-1 and JUN-1 control spermathecal valve dilation, along with the known role of FOS-1 in anchor cell invasion and cell fate specification in the uterus (Sherwood et al, 2005;Hwang et al, 2007;Oommen and Newman, 2007;Rimann and Hajnal, 2007;Sapir et al, 2007), establish C. elegans as a model for the control of reproduction by AP-1 proteins.…”

The Prdm family: expanding roles in stem cells and development

“…( Garriga et al, 1993;Hwang et al, 2007;Rimann and Hajnal, 2007 (Bjork et al, 2010;Chuikov et al, 2010;Kinameri et al, 2008) Tissue-specific expressions have not been described for Prdm2, Prdm5 and Prdm11. *For a complete description of the complex and dynamic expression patterns.…”

“…( Garriga et al, 1993;Hwang et al, 2007;Rimann and Hajnal, 2007) Drosophila ( ( Aguilo et al, 2011;Chuikov et al, 2010;Goyama et al, 2008;Hoyt et al, 1997;Parkinson et al, 2006;Sato et al, 2008;Zhang et al, 2011) Prdm8 Mouse: Axon targeting defects and axon tract loss 23 . (Ross et al, 2012) Prdm14 Mouse: Failure to upregulate multipotency and primordial germ cell-specific genes.…”

“…(Yamaji et al, 2008) ( Aguilo et al, 2011;Bjork et al, 2010;Chuikov et al, 2010;Kajimura et al, 2009;Seale et al, 2007;Seale et al, 2009) In C. elegans, EGL-43 (Fig. 1B,C) and Notch cooperate in two sequential signalling events during vulval development (Hwang et al, 2007;Rimann and Hajnal, 2007). Four precursor cells give rise to the vulva: one pair of cells directly adopts a ventral uterine precursor cell (VU) fate and the second pair undergoes a Notchmediated binary cell fate choice.…”

“…In the nascent VU cell, Notch is subsequently required to properly maintain EGL-43 expression. Finally, as the VU cells differentiate into  cells, Egl43 and Notch co-activate the lin-11 homeobox gene (Hwang et al, 2007;Rimann and Hajnal, 2007). EGL-43 is additionally required in a Notch-independent manner for AC invasion of the vulval epithelium.…”