Baboon/dSmad2 TGF-beta signaling is required during late larval stage for development of adult-specific neurons

UMMS Affiliation

Department of Neurobiology; Tzumin Lee Lab; Graduate School of Biomedical Sciences, Neuroscience Program

Publication Date


Document Type



Activin Receptors, Type I; Activin Receptors, Type II; Activins; Animals; Drosophila Proteins; Drosophila melanogaster; Larva; Metamorphosis, Biological; Morphogenesis; Mutation; Neurons; Protein-Serine-Threonine Kinases; Receptors, Transforming Growth Factor beta; Signal Transduction; Smad2 Protein; Transforming Growth Factor beta


Developmental Neuroscience


The intermingling of larval functional neurons with adult-specific neurons during metamorphosis contributes to the development of the adult Drosophila brain. To better understand this process, we characterized the development of a dorsal cluster (DC) of Atonal-positive neurons that are born at early larval stages but do not undergo extensive morphogenesis until pupal formation. We found that Baboon(Babo)/dSmad2-mediated TGF-beta signaling, known to be essential for remodeling of larval functional neurons, is also indispensable for proper morphogenesis of these adult-specific neurons. Mosaic analysis reveals slowed development of mutant DC neurons, as evidenced by delays in both neuronal morphogenesis and atonal expression. We observe similar phenomena in other adult-specific neurons. We further demonstrate that Babo/dSmad2 operates autonomously in individual neurons and specifically during the late larval stage. Our results suggest that Babo/dSmad2 signaling prior to metamorphosis may be widely required to prepare neurons for the dynamic environment present during metamorphosis.

DOI of Published Version



EMBO J. 2006 Feb 8;25(3):615-27. Epub 2006 Jan 26. Link to article on publisher's site

Journal/Book/Conference Title

The EMBO journal


Co-author Lei Shi is a student in the Neuroscience program in the Graduate School of Biomedical Sciences (GSBS) at UMass Medical School.

Related Resources

Link to Article in PubMed

PubMed ID