Jing: a downstream target of slbo required for developmental control of border cell migration.

TitleJing: a downstream target of slbo required for developmental control of border cell migration.
Publication TypeJournal Article
Year of Publication2001
AuthorsLiu Y, Montell DJ
JournalDevelopment
Volume128
Issue3
Pagination321-30
Date Published2001 Feb
ISSN0950-1991
KeywordsAdipocytes, Amino Acid Sequence, Animals, Cadherins, CCAAT-Enhancer-Binding Proteins, Cell Differentiation, Cell Movement, Cloning, Molecular, Drosophila melanogaster, Drosophila Proteins, Female, Gene Expression Regulation, Developmental, Genes, Reporter, Immunohistochemistry, Molecular Sequence Data, Mutation, Nuclear Proteins, Phenotype, Physical Chromosome Mapping, Repressor Proteins, RNA, Messenger, Sequence Homology, Amino Acid, Transcription Factors
Abstract

<p>Epithelial to mesenchymal transitions and cell migration are important features of embryonic development and tumor metastasis. We are employing a systematic genetic approach to study the border cells in the Drosophila ovary, as a simple model for these cellular behaviors. Previously we found that expression of the basic-region/leucine zipper transcription factor, C/EBP, is required for the border cells to initiate their migration. Here we report the identification of a second nuclear factor, named JING (which means 'still'), that is required for initiation of border cell migration. The jing locus was identified in a screen for mutations that cause border cell migration defects in mosaic clones. The jing mutant phenotype resembles that of slbo mutations, which disrupt the Drosophila C/EBP gene, but is distinct from other classes of border cell migration mutants. Expression of a jing-lacZ reporter in border cells requires C/EBP. Moreover, expression of jing from a heat-inducible promoter rescues the border cell migration defects of hypomorphic slbo mutants. The JING protein is most closely related to a mouse protein, AEBP2, which was identified on the basis of its ability to bind a small regulatory sequence within the adipocyte AP2 gene to which mammalian C/EBP also binds. We propose that the need to coordinate cell differentiation with nutritional status may be the link between mammalian adipocytes and Drosophila border cells that led to the conservation of C/EBP and AEBP2.</p>

Alternate JournalDevelopment
PubMed ID11152631
Grant ListR01 AG063907 / AG / NIA NIH HHS / United States