|
|
|
||||
| Home Help Feedback Subscriptions Archive Search | |||||
The fully linked HTML version of this article has now been published.
The genome of the social amoeba Dictyostelium discoideum encodes
JCS ePress
online publication date 27 Nov 2007
doi: 10.1242/jcs.012179
This Article ![]()
![]()
Full Text (PDF)
![]()
Supplementary Material
![]()
All Versions of this Article:
jcs.012179v1
120/24/4345
most recent![]()
Alert me when this article is cited
![]()
Alert me if a correction is posted
![]()
Services ![]()
![]()
Email this article to a friend
![]()
Similar articles in this journal
![]()
Similar articles in PubMed
![]()
Alert me to new issues of the journal
![]()
Download to citation manager
![]()
![]()
Citing Articles ![]()
![]()
Citing Articles via Google Scholar
![]()
Google Scholar ![]()
![]()
Articles by Rohlfs, M.
![]()
Articles by Schleicher, M.
![]()
Search for Related Content
![]()
PubMed ![]()
![]()
PubMed Citation
![]()
Articles by Rohlfs, M.
![]()
Articles by Schleicher, M.
Research Article
The Ste20-like kinase SvkA of Dictyostelium discoideum is essential for late stages of cytokinesis
* Author for correspondence (e-mail: schleicher{at}lrz.uni-muenchen.de)
285 kinases, which represents
2.6% of the total genome and suggests a signaling complexity similar to that of yeasts and humans. The behavior of D. discoideum as an amoeba and during development relies heavily on fast rearrangements of the actin cytoskeleton. Here, we describe the knockout phenotype of the svkA gene encoding severin kinase, a homolog of the human MST3, MST4 and YSK1 kinases. SvkA-knockout cells show drastic defects in cytokinesis, development and directed slug movement. The defect in cytokinesis is most prominent, leading to multinucleated cells sometimes with >30 nuclei. The defect arises from the frequent inability of svkA-knockout cells to maintain symmetry during formation of the cleavage furrow and to sever the last cytosolic connection. We demonstrate that GFP-SvkA is enriched at the centrosome and localizes to the midzone during the final stage of cell division. This distribution is mediated by the C-terminal half of the kinase, whereas a rescue of the phenotypic changes requires the active N-terminal kinase domain as well. The data suggest that SvkA is part of a regulatory pathway from the centrosome to the midzone, thus regulating the completion of cell division.
© The Company of Biologists Ltd 2007