The atypical mammalian ligand Delta-like homologue 1 (Dlk1) can regulate Notch signalling in Drosophila

Sarah J. Bray, Shuji Takada, Emma Harrison, Shing Chuan Shen, Anne C. Ferguson-Smith

研究成果: 雜誌貢獻文章

61 引文 (Scopus)

摘要

Background. Mammalian Delta-like 1 (Dlk-1) protein shares homology with Notch ligands but lacks a critical receptor-binding domain. Thus it is unclear whether it is able to interact with Notch in vivo. Unlike mammals, Drosophila have a single Notch receptor allowing a simple in vivo assay for mammalian Dlk1 function. Results. Here we show that membrane-bound DLK1 can regulate Notch leading to altered cellular distribution of Notch itself and inhibiting expression of Notch target genes. The resulting adult phenotypes are indicative of reduced Notch function and are enhanced by Notch mutations, confirming that DLK1 action is antagonistic. In addition, cells expressing an alternative Dlk1 isoform exhibit alterations in cell size, functions previously not attributed to Notch suggesting that DLK1 might also act via an alternative target. Conclusion. Our results demonstrate that DLK1 can regulate the Notch receptor despite its atypical structure.

原文英語
文章編號11
期刊BMC Developmental Biology
8
DOIs
出版狀態已發佈 - 2008
對外發佈Yes

指紋

Notch Receptors
Drosophila
Ligands
Cell Size
Mammals
Protein Isoforms
Phenotype
Mutation
Membranes
Genes
delta protein

ASJC Scopus subject areas

  • Medicine(all)

引用此文

The atypical mammalian ligand Delta-like homologue 1 (Dlk1) can regulate Notch signalling in Drosophila. / Bray, Sarah J.; Takada, Shuji; Harrison, Emma; Shen, Shing Chuan; Ferguson-Smith, Anne C.

於: BMC Developmental Biology, 卷 8, 11, 2008.

研究成果: 雜誌貢獻文章

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