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Regulation of the Yin Yang 1 transcr...

Gordon, Steven Jeffrey.

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Regulation of the Yin Yang 1 transcription factor binding to the murine 3' Igh enhancers hs3A and hs3B, by inducers of class switch recombination.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Regulation of the Yin Yang 1 transcription factor binding to the murine 3' Igh enhancers hs3A and hs3B, by inducers of class switch recombination./
作者:	Gordon, Steven Jeffrey.
面頁冊數:	151 p.
附註:	Adviser: Barbara K. Birshtein.
Contained By:	Dissertation Abstracts International64-03B.
標題:	Biology, Cell. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3086890

Regulation of the Yin Yang 1 transcription factor binding to the murine 3' Igh enhancers hs3A and hs3B, by inducers of class switch recombination.
Gordon, Steven Jeffrey.

Regulation of the Yin Yang 1 transcription factor binding to the murine 3' Igh enhancers hs3A and hs3B, by inducers of class switch recombination. - 151 p.

Adviser: Barbara K. Birshtein.

Thesis (Ph.D.)--Yeshiva University, 2003.

The 3<super>′</super> <italic>Igh</italic> enhancers, hs3B and/or hs4, are required for germline transcription (GT), and hence, class switch recombination (CSR) for multiple isotypes. A number of hs3-binding transcription factors have been identified by EMSA, including octamer and NF-kB family members, and Pax5. We have found that the binding of the transcription factor, Yin Yang 1 (YY1), to hs3 and to the μE1 site of the intronic enhancer, <italic> E</italic>μ, is induced in primary splenic B cells after &sim;48 hrs in response to LPS and other activators of CSR. Transient transfection experiments in B cell lines indicate that YY1 is an activator of hs3. Interestingly, levels of YY1 expression are unchanged in resting and LPS-stimulated B cells. Mixing experiments followed by EMSA showed that a protein present in resting B cells prevented YY1's binding to DNA. We found that recombinant Rb protein inhibited binding of YY1 to hs3 in a dose-dependent manner; and we have identified complexes of endogenous YY1 with the retinoblastoma protein (Rb) in resting B cells, but not in LPS stimulated B cells. A difference in Rb phosphorylation state was also confirmed between resting (G<sub>0</sub>) B cells and LPS stimulated B cells. These observations suggest that the interaction of YY1 with hypo-phosphorylated Rb in resting B cells prevents YY1's interaction with DNA. After stimulation with class switching activators, such as LPS, Rb becomes hyper-phosphorylated, YY1 is released and can then bind to the hs3 enhancer and <italic>E</italic>μ. Our data provide the first evidence for the role of YY1 in regulating hs3 enhancer activity, and suggest a mechanism by which cell cycle control and the early stages of class switch recombination, mediated by the 3<super>′ </super> <italic>Igh</italic> and intronic enhancers, can be linked at the molecular level.Subjects--Topical Terms:

1017686
Biology, Cell.

Regulation of the Yin Yang 1 transcription factor binding to the murine 3' Igh enhancers hs3A and hs3B, by inducers of class switch recombination.
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245 1 0 $a Regulation of the Yin Yang 1 transcription factor binding to the murine 3' Igh enhancers hs3A and hs3B, by inducers of class switch recombination.
300 $a 151 p.
500 $a Adviser: Barbara K. Birshtein.
500 $a Source: Dissertation Abstracts International, Volume: 64-03, Section: B, page: 1165.
502 $a Thesis (Ph.D.)--Yeshiva University, 2003.
520 $a The 3<super>′</super> <italic>Igh</italic> enhancers, hs3B and/or hs4, are required for germline transcription (GT), and hence, class switch recombination (CSR) for multiple isotypes. A number of hs3-binding transcription factors have been identified by EMSA, including octamer and NF-kB family members, and Pax5. We have found that the binding of the transcription factor, Yin Yang 1 (YY1), to hs3 and to the μE1 site of the intronic enhancer, <italic> E</italic>μ, is induced in primary splenic B cells after &sim;48 hrs in response to LPS and other activators of CSR. Transient transfection experiments in B cell lines indicate that YY1 is an activator of hs3. Interestingly, levels of YY1 expression are unchanged in resting and LPS-stimulated B cells. Mixing experiments followed by EMSA showed that a protein present in resting B cells prevented YY1's binding to DNA. We found that recombinant Rb protein inhibited binding of YY1 to hs3 in a dose-dependent manner; and we have identified complexes of endogenous YY1 with the retinoblastoma protein (Rb) in resting B cells, but not in LPS stimulated B cells. A difference in Rb phosphorylation state was also confirmed between resting (G<sub>0</sub>) B cells and LPS stimulated B cells. These observations suggest that the interaction of YY1 with hypo-phosphorylated Rb in resting B cells prevents YY1's interaction with DNA. After stimulation with class switching activators, such as LPS, Rb becomes hyper-phosphorylated, YY1 is released and can then bind to the hs3 enhancer and <italic>E</italic>μ. Our data provide the first evidence for the role of YY1 in regulating hs3 enhancer activity, and suggest a mechanism by which cell cycle control and the early stages of class switch recombination, mediated by the 3<super>′ </super> <italic>Igh</italic> and intronic enhancers, can be linked at the molecular level.
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