1: EMBO J. 2005 Aug 3;24(15):2753-67. Epub 2005 Jul 14. 

TAF4 inactivation in embryonic fibroblasts activates TGF beta signalling and
autocrine growth.

Mengus G, Fadloun A, Kobi D, Thibault C, Perletti L, Michel I, Davidson I.

Institut de Genetique et de Biologie Moleculaire et Cellulaire, CNRS/INSERM/ULP,
Illkirch, France.

We have inactivated transcription factor TFIID subunit TBP-associated factor 4
(TAF4) in mouse embryonic fibroblasts. Mutant taf4(-/-) cells are viable and
contain intact TFIID comprising the related TAF4b showing that TAF4 is not an
essential protein. TAF4 inactivation deregulates more than 1000 genes indicating
that TFIID complexes containing TAF4 and TAF4b have distinct target gene
specificities. However, taf4(-/-) cell lines have altered morphology and exhibit
serum-independent autocrine growth correlated with the induced expression of
several secreted mitotic factors and activators of the transforming growth
factor beta signalling pathway. In addition to TAF4 inactivation, many of these
genes can also be induced by overexpression of TAF4b. A competitive equilibrium
between TAF4 and TAF4b therefore regulates expression of genes controlling cell
proliferation. We have further identified a set of genes that are regulated both
by TAF4 and upon adaptation to serum starvation and which may be important
downstream mediators of serum-independent growth. Our study also shows that TAF4
is an essential cofactor for activation by the retinoic acid receptor and CREB,
but not for Sp1 and the vitamin D3 receptor.

PMID: 16015375 [PubMed - indexed for MEDLINE]


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2: Retrovirology. 2004 Jul 30;1(1):19. 

The expanding role of Tax in transcription.

de la Fuente C, Kashanchi F.

Department of Biochemistry and Molecular Biology, The George Washington
University School of Medicine, Washington, DC 20037, USA. bcmclf@gwumc.edu

The viral transactivator of HTLV-I, Tax, has long been shown to target the
earliest steps of transcription by forming quaternary complexes with sequence
specific transcription factors and histone-modifying enzymes in the LTR of
HTLV-I. However, a new study suggests that Tax preferentially transactivates the
21-bp repeats through CREB1 and not other bZIP proteins. The additional
transactivation of Tax-responsive promoters subsequent to initiation is also
presented. This result highlights a potentially novel role of Tax following TBP
recruitment (i.e. initiation) and may expand the mechanism of Tax
transactivation in promoter clearance and transcriptional elongation.

PMID: 15285790 [PubMed - in process]


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