4.4 Article

A network of PUF proteins and Ras signaling promote mRNA repression and oogenesis in C. elegans

期刊

DEVELOPMENTAL BIOLOGY
卷 366, 期 2, 页码 218-231

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ydbio.2012.03.019

关键词

Translational control; PUF protein; Oogenesis; RNA-binding protein; Ras; Map Kinase; ERK; Translation

资金

  1. National Institutes of Health National Center for Research Resources
  2. National Science Foundation [0725416]
  3. National Institutes of Health [R01 GM07968]
  4. Direct For Biological Sciences
  5. Division Of Integrative Organismal Systems [0725416] Funding Source: National Science Foundation

向作者/读者索取更多资源

Cell differentiation requires integration of gene expression controls with dynamic changes in cell morphology, function, and control. Post-transcriptional mRNA regulation and signaling systems are important to this process but their mechanisms and connections are unclear. During C. elegans oogenesis, we find that two groups of PUF RNA binding proteins (RNABPs), PUF-3/11 and PUF-5/6/7, control different specific aspects of oocyte formation. PUF-3/11 limits oocyte growth, while PUF-5/6/7 promotes oocyte organization and formation. These two PUF groups repress mRNA translation through overlapping but distinct sets of 3' untranslated regions (3'UTRs). Several PUF-dependent mRNAs encode other mRNA regulators suggesting both PUF groups control developmental patterning of mRNA regulation circuits. Furthermore, we find that the Ras-MapKinase/ERK pathway functions with PUF-5/6/7 to repress specific mRNAs and control oocyte organization and growth. These results suggest that diversification of PUF proteins and their integration with Ras-MAPK signaling modulates oocyte differentiation. Together with other studies, these findings suggest positive and negative interactions between the Ras-MAPK system and PUF RNA-binding proteins likely occur at multiple levels. Changes in these interactions over time can influence spatiotemporal patterning of tissue development. (C) 2012 Elsevier Inc. All rights reserved.

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