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Resources » Paper

Paula Checchi et al. (2006) Development & Evolution Meeting "emb-4 is a Highly Conserved Gene with a Role in Germline-Specific Chromatin Remodeling during C. elegans Embryogenesis"

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  • Comments on Paula Checchi et al. (2006) Development & Evolution Meeting "emb-4 is a Highly Conserved Gene with a Role in Germline-Specific Chromatin Remodeling during C. elegans Embryogenesis" (0)

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    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00027894

    Paula Checchi, & William Kelly (2006). emb-4 is a Highly Conserved Gene with a Role in Germline-Specific Chromatin Remodeling during C. elegans Embryogenesis presented in Development & Evolution Meeting. Unpublished information; cite only with author permission.

    Early embryogenesis in C. elegans is characterized by a series of asymmetric cellular divisions, resulting in somatic lineages sequentially separating from "P"-germ blastomeres. A number of protective mechanisms exist that appear to shield germline blastomeres from inductive signals that specify the fates of somatic cells. In one mechanism, germ cells are kept transcriptionally quiescent by the maternally loaded CCCH protein PIE-1. However, upon the birth of the germ cell precursors Z2 and Z3, PIE-1 disappears, yet Z2/Z3 remain quiescent. The mechanisms controlling the temporal regulation of PIE-1 in the nascent germ cells as well as subsequent repressive processes are poorly understood. We have previously demonstrated that there is a chromatin-based repression that succeeds PIE-1 degradation (Schaner et al., 2003). The chromatin in the primordial germ cells Z2/Z3 loses certain histone modifications including histone H3 K4 dimethylation, a conserved marker for transcriptionally competent chromatin. Here we show that mutations in emb-4 cause defects in both PIE-1 degradation and in germline-specific chromatin remodeling. We show that, as in early somatic blastomeres (Seydoux lab), the degradation of PIE-1 in Z2/Z3 is dependent upon the CCCH binding protein ZIF-1. In the absence of either zif-1 or emb-4, embryos abnormally retain PIE-1 in Z2/Z3. emb-4 is allelic to two previously identified mutants including sel-6, a suppressor of the lin-12(d) (Notch) mutant (Iskra Katic and Iva Greenwald, personal communication), and we have demonstrated that emb-4 encodes a highly conserved, novel protein with orthologs in fly, mouse, and human, for which functions have not been previously described. Currently we are investigating the molecular and genetic mechanisms that control PIE-1 degradation and germline-specific chromatin remodeling during embryogenesis.


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