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2014 ; 55
(9
): 1886-96
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The adipogenic transcriptional cofactor ZNF638 interacts with splicing regulators
and influences alternative splicing
#MMPMID25024404
Du C
; Ma X
; Meruvu S
; Hugendubler L
; Mueller E
J Lipid Res
2014[Sep]; 55
(9
): 1886-96
PMID25024404
show ga
Increasing evidence indicates that transcription and alternative splicing are
coordinated processes; however, our knowledge of specific factors implicated in
both functions during the process of adipocyte differentiation is limited. We
have previously demonstrated that the zinc finger protein ZNF638 plays a role as
a transcriptional coregulator of adipocyte differentiation via induction of PPAR?
in cooperation with CCAAT/enhancer binding proteins (C/EBPs). Here we provide new
evidence that ZNF638 is localized in nuclear bodies enriched with splicing
factors, and through biochemical purification of ZNF638's interacting proteins in
adipocytes and mass spectrometry analysis, we show that ZNF638 interacts with
splicing regulators. Functional analysis of the effects of ectopic ZNF638
expression on a minigene reporter demonstrated that ZNF638 is sufficient to
promote alternative splicing, a function enhanced through its recruitment to the
minigene promoter at C/EBP responsive elements via C/EBP proteins.
Structure-function analysis revealed that the arginine/serine-rich motif and the
C-terminal zinc finger domain required for speckle localization are necessary for
the adipocyte differentiation function of ZNF638 and for the regulation of the
levels of alternatively spliced isoforms of lipin1 and nuclear receptor
co-repressor 1. Overall, our data demonstrate that ZNF638 participates in
splicing decisions and that it may control adipogenesis through regulation of the
relative amounts of differentiation-specific isoforms.
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