Document Detail

Broad relays hormone signals to regulate stem cell differentiation in Drosophila midgut during metamorphosis.
MedLine Citation:
PMID:  23048182     Owner:  NLM     Status:  MEDLINE    
Like the mammalian intestine, the Drosophila adult midgut is constantly replenished by multipotent intestinal stem cells (ISCs). Although it is well known that adult ISCs arise from adult midgut progenitors (AMPs), relatively little is known about the mechanisms that regulate AMP specification. Here, we demonstrate that Broad (Br)-mediated hormone signaling regulates AMP specification. Br is highly expressed in AMPs temporally during the larva-pupa transition stage, and br loss of function blocks AMP differentiation. Furthermore, Br is required for AMPs to develop into functional ISCs. Conversely, br overexpression drives AMPs toward premature differentiation. In addition, we found that Br and Notch (N) signaling function in parallel pathways to regulate AMP differentiation. Our results reveal a molecular mechanism whereby Br-mediated hormone signaling directly regulates stem cells to generate adult cells during metamorphosis.
Xiankun Zeng; Steven X Hou
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Intramural    
Journal Detail:
Title:  Development (Cambridge, England)     Volume:  139     ISSN:  1477-9129     ISO Abbreviation:  Development     Publication Date:  2012 Nov 
Date Detail:
Created Date:  2012-10-10     Completed Date:  2012-12-20     Revised Date:  2013-11-05    
Medline Journal Info:
Nlm Unique ID:  8701744     Medline TA:  Development     Country:  England    
Other Details:
Languages:  eng     Pagination:  3917-25     Citation Subset:  IM    
The Mouse Cancer Genetics Program, Frederick National Laboratory for Cancer Research, National Institutes of Health, Frederick, MD 21702, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Cell Differentiation / genetics,  physiology*
Drosophila Proteins / genetics,  metabolism*
Gastrointestinal Tract / cytology,  metabolism*
Metamorphosis, Biological / genetics,  physiology
Receptors, Notch / genetics,  metabolism
Signal Transduction / genetics,  physiology
Stem Cells / cytology*,  metabolism
Transcription Factors / genetics,  metabolism*
Reg. No./Substance:
0/Drosophila Proteins; 0/Receptors, Notch; 0/Transcription Factors; 0/broad protein, Drosophila

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

Previous Document:  Combinatorial regulation of tissue specification by GATA and FOG factors.
Next Document:  Torso RTK controls Capicua degradation by changing its subcellular localization.