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TF2I is involved in chromatin remodeling during embryonic stem cell differentiation

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Abstract:

TFII-I proteins (TF2I and BEN) are multifunctional transcriptional factors regulating a number of genes during development, and their haploinsufficiency leads to the Williams-Beuren syndrome. We have generated TF2I and BEN knockout mice and demonstrated that inactivation of TFII-I genes do not change embryonic stem (ES) cell pluripotency but affects expression of specific sets of genes in all three germ layers. Our microarray and qRT-PCR studies indicate that TF2I (but not BEN) regulates expression of an unexpectedly large portion of chromatin-modified enzymes. Namely, TF2I KO results in significant decrease in expression of components of Polycomb Repressive Complex 2 (PRC2) Ezh2 and Eed. TF2I KO is also accompanied by both down-regulation of Setdb1 and Suv39h1 methylating H3K9 but shows up-regulation of Aof2 demethylating H3K4. This suggests specific changes in the methylation pattern of histone H3. Similarly, TF2I KO down-regulates histone arginine methyltransferases Prmt1 and Carm1 but has no effect on expression of none-histone arginine methyltransferases Prmt2 and Prmt3. In addition, TF2I KO leads to down-regulation of the distinct subsets of class II histone deacetilases (Hdac6 and Hdac9) and to a lesser extent class I histone deacetilases (Hdac1, Hdac2, and Hdac3) and histone acetyltransferases (Gcn5l2, Htatip, and Atf2). We have detected dramatic increase in expression of replacement histone variant H3.3B in TF2I KO embryos, which is consistent with significant alterations of histone H3 modifications.
TF2I-dependent changes in chromatin structure have been detected as early as in differentiating ES cells: during in vitro differentiation of murine ES cells, post-transcriptional silencing (knockdown) of TF2I by gene-specific siRNAs results in significant decrease in H3K27me3 of HOXA gene cluster (known targets of PRC2). Analysis of other Polycomb target genes in differentiating ES cells as well as TF2I-dependent changes in methylation at H3K36, at H3K4, and in histone acethylation is currently in progress.
Taken together, all above findings indicate that TF2I is required for maintaining the correct spatial and temporal expression of a specific group of epigenetic marker genes and, therefore, modulates embryonic developmental program by changing the histone code of target genes at very early stages of development.
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Association:
Name: Connecticut's Stem Cell Research International Symposium
URL:
http://stemconn.org


Citation:
URL: http://citation.allacademic.com/meta/p367117_index.html
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MLA Citation:

Makeyev, Aleksandr., Chimge, Nyam-Osor., Enkhmandakh, Badam. and Bayarsaihan, Dashzeveg. "TF2I is involved in chromatin remodeling during embryonic stem cell differentiation" Paper presented at the annual meeting of the Connecticut's Stem Cell Research International Symposium, Omni Hotel, New Haven, CT, Mar 23, 2009 <Not Available>. 2014-11-29 <http://citation.allacademic.com/meta/p367117_index.html>

APA Citation:

Makeyev, A. , Chimge, N. , Enkhmandakh, B. and Bayarsaihan, D. , 2009-03-23 "TF2I is involved in chromatin remodeling during embryonic stem cell differentiation" Paper presented at the annual meeting of the Connecticut's Stem Cell Research International Symposium, Omni Hotel, New Haven, CT <Not Available>. 2014-11-29 from http://citation.allacademic.com/meta/p367117_index.html

Publication Type: Poster
Review Method: Peer Reviewed
Abstract: TFII-I proteins (TF2I and BEN) are multifunctional transcriptional factors regulating a number of genes during development, and their haploinsufficiency leads to the Williams-Beuren syndrome. We have generated TF2I and BEN knockout mice and demonstrated that inactivation of TFII-I genes do not change embryonic stem (ES) cell pluripotency but affects expression of specific sets of genes in all three germ layers. Our microarray and qRT-PCR studies indicate that TF2I (but not BEN) regulates expression of an unexpectedly large portion of chromatin-modified enzymes. Namely, TF2I KO results in significant decrease in expression of components of Polycomb Repressive Complex 2 (PRC2) Ezh2 and Eed. TF2I KO is also accompanied by both down-regulation of Setdb1 and Suv39h1 methylating H3K9 but shows up-regulation of Aof2 demethylating H3K4. This suggests specific changes in the methylation pattern of histone H3. Similarly, TF2I KO down-regulates histone arginine methyltransferases Prmt1 and Carm1 but has no effect on expression of none-histone arginine methyltransferases Prmt2 and Prmt3. In addition, TF2I KO leads to down-regulation of the distinct subsets of class II histone deacetilases (Hdac6 and Hdac9) and to a lesser extent class I histone deacetilases (Hdac1, Hdac2, and Hdac3) and histone acetyltransferases (Gcn5l2, Htatip, and Atf2). We have detected dramatic increase in expression of replacement histone variant H3.3B in TF2I KO embryos, which is consistent with significant alterations of histone H3 modifications.
TF2I-dependent changes in chromatin structure have been detected as early as in differentiating ES cells: during in vitro differentiation of murine ES cells, post-transcriptional silencing (knockdown) of TF2I by gene-specific siRNAs results in significant decrease in H3K27me3 of HOXA gene cluster (known targets of PRC2). Analysis of other Polycomb target genes in differentiating ES cells as well as TF2I-dependent changes in methylation at H3K36, at H3K4, and in histone acethylation is currently in progress.
Taken together, all above findings indicate that TF2I is required for maintaining the correct spatial and temporal expression of a specific group of epigenetic marker genes and, therefore, modulates embryonic developmental program by changing the histone code of target genes at very early stages of development.


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