Alterations in ribosome biogenesis cause specific defects in C. elegans hermaphrodite gonadogenesis
- 作者：Roumen Voutev ; Darrell J. Killian ; James Hyungsoo Ahn and E. Jane Albert Hubbard
- 关键词：Gonadogenesis ; Proximal germline tumor ; Ribosome biogenesis ; LIN-35/Rb
- 刊名：Developmental Biology
- 出版年：2006
- 期刊代码：167_00121606
- 类别：bio
- 出版时间：1 October 2006
- 卷：298
- 期：1
- 页码：45-58
- 文件大小：1502 K
摘要
Ribosome biogenesis is a cell-essential process that influences cell growth, proliferation, and differentiation. How ribosome biogenesis impacts development, however, is poorly understood. Here, we establish a link between ribosome biogenesis and gonadogenesis in Caenorhabditis elegans that affects germline proliferation and patterning. Previously, we determined that pro-1(+)activity is required in the soma – specifically, the sheath/spermatheca sublineage – to promote normal proliferation and prevent germline tumor formation. Here, we report that PRO-1, like its yeast ortholog IPI3, influences rRNA processing. pro-1tumors are suppressed by mutations in ncl-1or lin-35/Rb, both of which elevate pre-rRNA levels. Thus, in this context, lin-35/Rbacts as a soma-autonomous germline tumor promoter. We further report the characterization of two additional genes identified for their germline tumor phenotype, pro-2and pro-3, and find that they, too, encode orthologs of proteins involved in ribosome biogenesis in yeast (NOC2 and SDA1, respectively). Finally, we demonstrate that depletion of additional C. elegansorthologs of yeast ribosome biogenesis factors display phenotypes similar to depletion of progenes. We conclude that the C. elegansdistal sheath is particularly sensitive to alterations in ribosome biogenesis and that ribosome biogenesis defects in one tissue can non-autonomously influence proliferation in an adjacent tissue.