Affiliation: Southern Connecticut State University
Keywords: n. networks; c. TGFbeta
Given its pleiotropic nature, TGF-b signaling must be precisely regulated both intra- and extracellularly to have the proper effect on target cells. Inhibitory SMADs (I-SMADs) are a potent intracellular regulator of TGF-b signaling. However, there are numerous hypotheses regarding the mechanism by which I-SMADs function. Although biochemical studies show that Dad, the sole Drosophila I-SMAD, inhibits the receptors that phosphorylate the effector molecule Mad, our in vivo results indicate that Dad functions downstream of the receptors. We have found a paradoxical increase in phosphorylated Mad (pMad) in motor nuclei following Dad overexpression. qPCR analysis supports the hypothesis that a homeostatic transcriptional response counteracts I-SMAD activity in motor neurons.