Document Detail


TLP-1 is an asymmetric cell fate determinant that responds to Wnt signals and controls male tail tip morphogenesis in C. elegans.
MedLine Citation:
PMID:  11880358     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We have isolated mutations defining a new gene, tlp-1, that affect asymmetric cell fates and morphogenesis during the development of the C. elegans tail. tlp-1 mutations cause defects in the specification of asymmetric cell fates in the descendants of the T blast cell, whose polarity is controlled by Wnt signaling and cause abnormal male tail development leading to the formation of a posterior protrusion reminiscent of 'leptoderan', or pointy tailed, nematode species. In wild-type C. elegans males, which have a 'peloderan' or rounded tail, retraction of the tail tip hypodermis involves a temporally ordered set of cell fusions and changes in cell shape that appear to be heterochronically delayed in tlp-1 males, suggesting that subtle changes in these events can bring about evolutionary changes in morphology. tlp-1 encodes a C2H2 zinc-finger protein that is a member of the Sp family of transcription factors. A TLP-1::GFP fusion protein is expressed in the nuclei of many cells during early embryogenesis and then becomes restricted primarily to posterior cells. At hatching, it is expressed in several head neurons, the posterior intestine cells, tail hypodermal cells, the T cells and specific T-cell descendents in a pattern that suggests TLP-1 may be asymmetrically expressed during the divisions of the T cell lineage. Furthermore, the asymmetry of TLP-1 expression and function appears to be controlled by Wnt signals that control T cell polarity. These results suggest that tlp-1 encodes a transcription factor required for cellular asymmetry that functions downstream of Wnt signals that control cell polarity, as well as in cell fusion and patterning in the C. elegans tail.
Authors:
Xiaojun Zhao; Ying Yang; David H A Fitch; Michael A Herman
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Development (Cambridge, England)     Volume:  129     ISSN:  0950-1991     ISO Abbreviation:  Development     Publication Date:  2002 Mar 
Date Detail:
Created Date:  2002-03-06     Completed Date:  2002-04-19     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8701744     Medline TA:  Development     Country:  England    
Other Details:
Languages:  eng     Pagination:  1497-508     Citation Subset:  IM    
Affiliation:
Program in Molecular, Cellular and Developmental Biology, Division of Biology, Kansas State University, Manhattan, KS 66506, USA.
Data Bank Information
Bank Name/Acc. No.:
GENBANK/AY046083
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MeSH Terms
Descriptor/Qualifier:
Animals
Caenorhabditis elegans / embryology*,  genetics*
Caenorhabditis elegans Proteins / genetics*
Cell Lineage / genetics
Cell Polarity / genetics
Cloning, Molecular
Gene Expression Regulation, Developmental*
Male
Molecular Sequence Data
Morphogenesis
Mutation
Proto-Oncogene Proteins / genetics,  physiology*
Signal Transduction / genetics
T-Lymphocytes / physiology
Tail / embryology
Transcription Factors / genetics*
Wnt Proteins
Zebrafish Proteins*
Grant Support
ID/Acronym/Agency:
GM56339/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/Caenorhabditis elegans Proteins; 0/Proto-Oncogene Proteins; 0/TLP-1 protein, Caenorhabditis elegans; 0/Transcription Factors; 0/Wnt Proteins; 0/Zebrafish Proteins

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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