SUMO Proteins are not Involved in TGF-β1-induced, Smad3/4-mediated Germline α Transcription, but PIASy Suppresses it in CH12F3-2A B Cells
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TGF-β induces IgA class switching by B cells. We previouslyreported that Smad3 and Smad4, pivotal TGF-β signal-transducing transcription factors, mediate germline (GL)α transcription induced by TGF-β1, resulting in IgA switchingby mouse B cells. Post-translational sumoylation ofSmad3 and Smad4 regulates TGF-β-induced transcriptionalactivation in certain cell types. In the present study, we investigatedthe effect of sumoylation on TGF-β1-induced,Smad3/4-mediated GLα transcription and IgA switching bymouse B cell line, CH12F3-2A. Overexpression of small ubiquitin-like modifier (SUMO)-1, SUMO-2 or SUMO-3 did notaffect TGF-β1-induced, Smad3/4-mediated GLα promoteractivity, expression of endogenous GLα transcripts, surfaceIgA expression, and IgA production. Next, we tested the effectof the E3 ligase PIASy on TGF-β1-induced, Smad3/4-mediated GLα promoter activity. We found that PIASy overexpressionsuppresses the GLα promoter activity in cooperationwith histone deacetylase 1. Taken together, these resultssuggest that SUMO itself does not affect regulation ofGLα transcription and IgA switching induced by TGF-β1/Smad3/4, while PIASy acts as a repressor.
Abstract
TGF-β induces IgA class switching by B cells. We previouslyreported that Smad3 and Smad4, pivotal TGF-β signal-transducing transcription factors, mediate germline (GL)α transcription induced by TGF-β1, resulting in IgA switchingby mouse B cells. Post-translational sumoylation ofSmad3 and Smad4 regulates TGF-β-induced transcriptionalactivation in certain cell types. In the present study, we investigatedthe effect of sumoylation on TGF-β1-induced,Smad3/4-mediated GLα transcription and IgA switching bymouse B cell line, CH12F3-2A. Overexpression of small ubiquitin-like modifier (SUMO)-1, SUMO-2 or SUMO-3 did notaffect TGF-β1-induced, Smad3/4-mediated GLα promoteractivity, expression of endogenous GLα transcripts, surfaceIgA expression, and IgA production. Next, we tested the effectof the E3 ligase PIASy on TGF-β1-induced, Smad3/4-mediated GLα promoter activity. We found that PIASy overexpressionsuppresses the GLα promoter activity in cooperationwith histone deacetylase 1. Taken together, these resultssuggest that SUMO itself does not affect regulation ofGLα transcription and IgA switching induced by TGF-β1/Smad3/4, while PIASy acts as a repressor.
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