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KMID : 0923620140140060321
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Immune Network
2014 Volume.14 No. 6 p.321 ~ p.327
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SUMO Proteins are not Involved in TGF-β-induced, Smad3/4-mediated Germline α Transcription, but PIASy Suppresses it in CH12F3-2A B Cells
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Lee Sang-Hoon
Kim Pyeung-Hyeun
Oh Sang-Muk
Park Jung-Hwan
Yoo Yung-Choon
Lee Jung-Lim
Park Seok-Rae
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Abstract
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TGF-β induces IgA class switching by B cells. We previously reported that Smad3 and Smad4, pivotal TGF-β signal- transducing transcription factors, mediate germline (GL) α transcription induced by TGF-?1, resulting in IgA switching by mouse B cells. Post-translational sumoylation of Smad3 and Smad4 regulates TGF-?-induced transcriptional activation in certain cell types. In the present study, we investigated the effect of sumoylation on TGF-?1-induced, Smad3/4-mediated GL? 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-?1-induced, Smad3/4-mediated GL? promoter activity, expression of endogenous GL? transcripts, surface IgA expression, and IgA production. Next, we tested the effect of the E3 ligase PIASy on TGF-?1-induced, Smad3/4- mediated GL? promoter activity. We found that PIASy overexpression suppresses the GL? promoter activity in cooperation with histone deacetylase 1. Taken together, these results suggest that SUMO itself does not affect regulation of GL? transcription and IgA switching induced by TGF-?1/ Smad3/4, while PIASy acts as a repressor.
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KEYWORD
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IgA, germline α transcripts, SUMO, PIASy, HDAC1
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