emb-4 is a conserved gene required for efficient germline-specific chromatin remodeling during Caenorhabditis elegans embryogenesis.

Authors:
Checchi PM, Kelly WG
Associated Labs:
Kelly Lab (Emory University)
Genetics. 2006 Dec . 174(4):1895-906.
PMID: 17028322
In C. elegans, germline blastomeres are initially kept transcriptionally quiescent by the maternally loaded CCCH zinc-finger protein PIE-1. PIE-1 disappears upon the birth of the primordial germ cells Z2 and Z3, yet these cells appear to remain quiescent. We have previously demonstrated that there is a chromatin-based repression that succeeds PIE-1 degradation. The chromatin in Z2/Z3 loses certain histone modifications, including histone H3 lysine 4 dimethylation (H3K4me2), a conserved marker for transcriptionally competent chromatin. We find that mutations in the maternal-effect gene emb-4 cause defects in both PIE-1 degradation and germline-specific chromatin remodeling. emb-4 encodes a highly conserved protein with orthologs in fly, mouse, and human and has a subtle role in Notch signaling. The embryonic phenotype of emb-4 is consistent with a defect in the efficient and timely activation of developmental programs, including germline chromatin remodeling. We also find that, as in early somatic blastomeres, the degradation of PIE-1 in Z2/Z3 is facilitated by zinc-finger-interacting protein ZIF-1, and in the absence of either zif-1 or emb-4, PIE-1 is abnormally retained in Z2/Z3.

Want to be recognized as an author of this publication?

Create your LabLife profile and tag yourself! You will also be able to tag other authors after you log into your account.

Create New Account

Login

What is LabLife?

LabLife is a collection of tools to help scientists organize, share and discover.

Learn more