LIN-23, an E3 Ubiquitin Ligase Component, Is Required for the Repression of CDC-25.2 Activity during Intestinal Development in Caenorhabditis elegans

( ) utilizes two different cell-cycle modes, binucleations during the L1 larval stage and endoreduplications at four larval moltings, for its postembryonic intestinal development. Previous genetic studies indicated that CDC-25.2 is specifically required for binucleations at the L1 larval stage and i...

Full description

Saved in:
Bibliographic Details
Published inMolecules and cells Vol. 39; no. 11; pp. 834 - 840
Main Authors Son, Miseol, Kawasaki, Ichiro, Oh, Bong-Kyeong, Shim, Yhong-Hee
Format Journal Article
LanguageEnglish
Published United States Korean Society for Molecular and Cellular Biology 30.11.2016
한국분자세포생물학회
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:( ) utilizes two different cell-cycle modes, binucleations during the L1 larval stage and endoreduplications at four larval moltings, for its postembryonic intestinal development. Previous genetic studies indicated that CDC-25.2 is specifically required for binucleations at the L1 larval stage and is repressed before endoreduplications. Furthermore, LIN-23, the β-TrCP ortholog, appears to function as a repressor of CDC-25.2 to prevent excess intestinal divisions. We previously reported that intestinal hyperplasia in mutants was effectively suppressed by the RNAi depletion of . Nevertheless, LIN-23 targeting CDC-25.2 for ubiquitination as a component of E3 ubiquitin ligase has not yet been tested. In this study, LIN-23 is shown to be the major E3 ubiquitin ligase component, recognizing CDC-25.2 to repress their activities for proper transition of cell-cycle modes during the postembryonic intestinal development. In addition, for the first time that LIN-23 physically interacts with both CDC-25.1 and CDC-25.2 and facilitates ubiquitination for timely regulation of their activities during the intestinal development.
Bibliography:G704-000079.2016.39.11.002
ISSN:1016-8478
0219-1032
DOI:10.14348/molcells.2016.0238