Medical College of Wisconsin
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A genetic screen for modifiers of Drosophila decapentaplegic signaling identifies mutations in punt, Mothers against dpp and the BMP-7 homologue, 60A. Development 1998 May;125(9):1759-68

Date

06/12/1998

Pubmed ID

9521913

DOI

10.1242/dev.125.9.1759

Scopus ID

2-s2.0-0031860761 (requires institutional sign-in at Scopus site)   52 Citations

Abstract

decapentaplegic (dpp) is a Transforming Growth Factor beta (TGF-beta)-related growth factor that controls multiple developmental processes in Drosophila. To identify components involved in dpp signaling, we carried out a genetic screen for dominant enhancer mutations of a hypomorphic allele of thick veins (tkv), a type I receptor for dpp. We recovered new alleles of tkv, punt, Mothers against dpp (Mad) and Medea (Med), all of which are known to mediate dpp signaling. We also recovered mutations in the 60A gene which encodes another TGF-beta-related factor in Drosophila. DNA sequence analysis established that all three 60A alleles were nonsense mutations in the prodomain of the 60A polypeptide. These mutations in 60A caused defects in midgut morphogenesis and fat body differentiation. We present evidence that when dpp signaling is compromised, lowering the level of 60A impairs several dpp-dependent developmental processes examined, including the patterning of the visceral mesoderm, the embryonic ectoderm and the imaginal discs. These results provide the first in vivo evidence for the involvement of 60A in the dpp pathway. We propose that 60A activity is required to maintain optimal signaling capacity of the dpp pathway, possibly by forming biologically active heterodimers with Dpp proteins.

Author List

Chen Y, Riese MJ, Killinger MA, Hoffmann FM



MESH terms used to index this publication - Major topics in bold

Activin Receptors
Animals
Bone Morphogenetic Protein 7
Bone Morphogenetic Proteins
DNA Mutational Analysis
DNA-Binding Proteins
Drosophila
Drosophila Proteins
Genetic Complementation Test
Insect Proteins
Mesoderm
Mutation
Phenotype
Receptors, Cell Surface
Receptors, Growth Factor
Repressor Proteins
Signal Transduction
Smad4 Protein
Trans-Activators
Transcription Factors
Transforming Growth Factor beta