Document Detail

HMG-17 is an early marker of inductive interactions in the developing mouse kidney.
MedLine Citation:
PMID:  11683498     Owner:  NLM     Status:  MEDLINE    
We studied the relationship between proliferation, differentiation, and the expression of high-mobility-group protein 17 (HMG-17) during metanephric kidney development. Proliferating cells were found homogenously throughout the early kidney rudiment. The expression pattern of HMG-17 mRNA, on the other hand, was distinctly uneven: In the undifferentiated mesenchyme, the cells in the cranial "tail" part of the mesenchyme showed only a weak signal, whereas a group of cells lying close to the tip of the ureteric bud showed strong HMG-17 expression. The region distinctly positive for HMG-17 is known to contain the first cells to undergo mesenchyme-to-epithelium transition. Using the transfilter model system, strong expression of HMG-17 mRNA, followed by mesenchyme-to-epithelium transition, could be induced also in the "tail" part of the mesenchyme. The upregulation of HMG-17 in the metanephrogenic mesenchyme thus results from interaction with an inductor tissue. Throughout the renal development, the HMG-17 mRNA was also abundant in those epithelial and mesenchymal cells that were undergoing active cell differentiation, and the transcript was downregulated in mature cells. HMG-17 expression thus correlated with the processes of induction and differentiation rather than with proliferation. The present results suggest that HMG-17 could have a role in the activation of the genes regulating kidney organogenesis.
S Lehtonen; E Lehtonen
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Differentiation; research in biological diversity     Volume:  67     ISSN:  0301-4681     ISO Abbreviation:  Differentiation     Publication Date:  2001 Jun 
Date Detail:
Created Date:  2001-10-30     Completed Date:  2002-01-17     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0401650     Medline TA:  Differentiation     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  154-63     Citation Subset:  IM    
Department of Pathology, Haartman Institute University of Helsinki, Finland.
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MeSH Terms
Biological Markers / analysis
Cell Division
Embryonic Induction* / genetics
Embryonic and Fetal Development
Gene Expression Profiling
HMGN2 Protein / genetics,  metabolism*
In Situ Hybridization
Kidney / cytology,  embryology*,  growth & development,  metabolism*
Mesoderm / cytology,  metabolism
RNA, Messenger / genetics,  metabolism
Reg. No./Substance:
0/Biological Markers; 0/HMGN2 Protein; 0/RNA, Messenger

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