Differential Effects of Drosophila Mastermind on Asymmetric Cell Fate Specification and Neuroblast Formation

Barry Yedvobnick, Anumeha Kumar, Padmashree Chaudhury, Jonathan Opraseuth, Nathan Mortimer, Krishna Moorthi Bhat

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


During neurogenesis in the ventral nerve cord of the Drosophila embryo, Notch signaling participates in the pathway that mediates asymmetric fate specification to daughters of secondary neuronal precursor cells. In the NB4-2 → GMC-1 → RP2/sib lineage, a well-studied neuronal lineage in the ventral nerve cord, Notch signaling specifies sib fate to one of the daughter cells of GMC-1. Notch mediates this process via Mastermind (Mam). Loss of function for mam, similar to loss of function for Notch, results in GMC-1 symmetrically dividing to generate two RP2 neurons. Loss of function for mam also results in a severe neurogenic phenotype. In this study, we have undertaken a functional analysis of the Mam protein. We show that while ectopic expression of a truncated Mam protein induces a dominant-negative neurogenic phenotype, it has no effect on asymmetric fate specification. This truncated Mam protein rescues the loss of asymmetric specification phenotype in mam in an allele-specific manner. We also show an interallelic complementation of loss-of-asymmetry defect. Our results suggest that Mam proteins might associate during the asymmetric specification of cell fates and that the N-terminal region of the protein plays a role in this process.

Original languageEnglish (US)
Pages (from-to)1281-1289
Number of pages9
Issue number3
StatePublished - Mar 2004
Externally publishedYes

ASJC Scopus subject areas

  • General Medicine


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