TGF-${eta}$ induces IgA class switching by B cells. We previously reported that Smad3 and Smad4, pivotal TGF-${eta}$ signal-transducing transcription factors, mediate germline (GL) ${alpha}$ transcription induced by TGF-${eta}1$, resulting in IgA switching by mouse B cells. Post-translational sumoylation of Smad3 and Smad4 regulates TGF-${eta}$-induced transcriptional activation in certain cell types. In the present study, we investigated the effect of sumoylation on TGF-${eta}1$-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-${eta}1$-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-${eta}1$-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-${eta}1$/Smad3/4, while PIASy acts as a repressor.