• IMMUNE NETWORK
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• v.14 no.6
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• pp.321-327
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• 2014

TGF-${\beta}$ induces IgA class switching by B cells. We previously reported that Smad3 and Smad4, pivotal TGF-${\beta}$ signal-transducing transcription factors, mediate germline (GL) ${\alpha}$ transcription induced by TGF-${\beta}1$, resulting in IgA switching by mouse B cells. Post-translational sumoylation of Smad3 and Smad4 regulates TGF-${\beta}$-induced transcriptional activation in certain cell types. In the present study, we investigated the effect of sumoylation on TGF-${\beta}1$-induced, Smad3/4-mediated $GL{\alpha}$ transcription and IgA switching by mouse B cell line, CH12F3-2A. Overexpression of small ubiquitin-like modifier (SUMO)-1, SUMO-2 or SUMO-3 did not affect TGF-${\beta}1$-induced, Smad3/4-mediated $GL{\alpha}$ promoter activity, expression of endogenous $GL{\alpha}$ transcripts, surface IgA expression, and IgA production. Next, we tested the effect of the E3 ligase PIASy on TGF-${\beta}1$-induced, Smad3/4-mediated $GL{\alpha}$ promoter activity. We found that PIASy overexpression suppresses the $GL{\alpha}$ promoter activity in cooperation with histone deacetylase 1. Taken together, these results suggest that SUMO itself does not affect regulation of $GL{\alpha}$ transcription and IgA switching induced by TGF-${\beta}1$/Smad3/4, while PIASy acts as a repressor.