TY - JOUR
T1 - Genetic requirements for PIE-1 localization and inhibition of gene expression in the embryonic germ lineage of Caenorhabditis elegans
AU - Tenenhaus, Christina
AU - Schubert, Charlotte
AU - Seydoux, Geraldine
N1 - Funding Information:
We are especially grateful to Jim Priess, in whose laboratory the PIE-1 antibody was generated, and to Andy Fire, in whose laboratory the pie-1 in situ hybridization experiments were performed. We also thank Elisabeth Wayner for her assistance in the production of monoclonal antibodies; Lisa Timmons and Andy Fire for sharing unpublished results; Steve Warren, Craig Mello, and the Developmental Studies Hybridoma Bank (Johns Hopkins University and University of Iowa) for antibodies; the Caenorhabditis Genetics Center (funded by the NIH Center for Research Resources) for strains; and Bruce Bowerman, Andy Golden, Andy Fire, Jill Schumacher, and the anonymous reviewers for valuable com- ments on the manuscript. This work was supported by grants from the March of Dimes, the Packard Foundation, and the Searle Scholars Program/Chicago Community Trust.
PY - 1998/8/15
Y1 - 1998/8/15
N2 - In early Caenorhabditis elegans embryos, production of new mRNAs is inhibited in the germ lineage. This inhibition requires the germline factor PIE-1, and correlates with the absence in germline blastomeres of a phosphoepitope on RNA polymerase II (RNAPII-H5). We show that PIE-1 is uniformly distributed in oocytes and newly fertilized eggs, and becomes localized asymmetrically in the late one-cell stage. To begin to dissect the mechanisms required for PIE-1 localization and inhibition of RNAPII-H5 expression, we have examined the distribution of PIE-1 and RNAPII-H5 in maternal-effect mutants that disrupt embryonic development. We find that mutants that disrupt the asymmetric divisions of germline blastomeres mislocalize PIE-1, and activate RNAPII-H5 expression in the germ lineage. In contrast, mutants that alter somatic cell identities do not affect PIE-1 localization or RNAPII-H5 expression. Our observations suggest that PIE-1 represses mRNA transcription in each germline blastomere in a concentration- dependent manner. We also show that in wild-type, and in mutants where PIE-1 is mislocalized, the cellular and subcellular distribution of PIE-1 remarkably parallels that of the P granules, suggesting that the localizations of these two germline components are coordinately regulated.
AB - In early Caenorhabditis elegans embryos, production of new mRNAs is inhibited in the germ lineage. This inhibition requires the germline factor PIE-1, and correlates with the absence in germline blastomeres of a phosphoepitope on RNA polymerase II (RNAPII-H5). We show that PIE-1 is uniformly distributed in oocytes and newly fertilized eggs, and becomes localized asymmetrically in the late one-cell stage. To begin to dissect the mechanisms required for PIE-1 localization and inhibition of RNAPII-H5 expression, we have examined the distribution of PIE-1 and RNAPII-H5 in maternal-effect mutants that disrupt embryonic development. We find that mutants that disrupt the asymmetric divisions of germline blastomeres mislocalize PIE-1, and activate RNAPII-H5 expression in the germ lineage. In contrast, mutants that alter somatic cell identities do not affect PIE-1 localization or RNAPII-H5 expression. Our observations suggest that PIE-1 represses mRNA transcription in each germline blastomere in a concentration- dependent manner. We also show that in wild-type, and in mutants where PIE-1 is mislocalized, the cellular and subcellular distribution of PIE-1 remarkably parallels that of the P granules, suggesting that the localizations of these two germline components are coordinately regulated.
KW - CTD phosphorylation
KW - Caenorhabditis elegans
KW - Germline
KW - P granules
KW - PIE-1
KW - RNA polymerase II
KW - Transcriptional repression
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U2 - 10.1006/dbio.1998.8940
DO - 10.1006/dbio.1998.8940
M3 - Article
C2 - 9705228
AN - SCOPUS:0032529361
SN - 0012-1606
VL - 200
SP - 212
EP - 224
JO - Developmental biology
JF - Developmental biology
IS - 2
ER -