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  • Mice, Transgenic  (2)
  • American Association for the Advancement of Science (AAAS)  (2)
  • American Institute of Physics (AIP)
  • 1
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    Repression of the transcription factor Th-POK by Runx complexes in cytotoxic T cell development (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-02-09
    Description: Mouse CD4+CD8+ double-positive (DP) thymocytes differentiate into CD4+ helper-lineage cells upon expression of the transcription factor Th-POK but commit to the CD8+ cytotoxic lineage in its absence. We report the redirected differentiation of class I-restricted thymocytes into CD4+CD8- helper-like T cells upon loss of Runx transcription factor complexes. A Runx-binding sequence within the Th-POK locus acts as a transcriptional silencer that is essential for Th-POK repression and for development of CD8+ T cells. Thus, Th-POK expression and genetic programming for T helper cell development are actively inhibited by Runx-dependent silencer activity, allowing for cytotoxic T cell differentiation. Identification of the transcription factors network in CD4 and CD8 lineage choice provides insight into how distinct T cell subsets are developed for regulating the adaptive immune system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Setoguchi, Ruka -- Tachibana, Masashi -- Naoe, Yoshinori -- Muroi, Sawako -- Akiyama, Kaori -- Tezuka, Chieko -- Okuda, Tsukasa -- Taniuchi, Ichiro -- New York, N.Y. -- Science. 2008 Feb 8;319(5864):822-5. doi: 10.1126/science.1151844.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Transcriptional Regulation, RIKEN Research Center for Allergy and Immunology, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama 230-0045, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18258917" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Lineage ; Chromatin Immunoprecipitation ; Core Binding Factor Alpha 2 Subunit/genetics/*physiology ; Core Binding Factor Alpha 3 Subunit/genetics/*physiology ; Core Binding Factor beta Subunit/metabolism ; Histocompatibility Antigens Class I/immunology ; Histocompatibility Antigens Class II/immunology ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Silencer Elements, Transcriptional ; T-Lymphocyte Subsets/cytology/*immunology/metabolism ; T-Lymphocytes, Cytotoxic/cytology/*immunology/metabolism ; T-Lymphocytes, Helper-Inducer/cytology/immunology/metabolism ; Transcription Factors/genetics/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Epigenetic regulation of mouse sex determination by the histone demethylase Jmjd1a (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-09-07
    Description: Developmental gene expression is defined through cross-talk between the function of transcription factors and epigenetic status, including histone modification. Although several transcription factors play crucial roles in mammalian sex determination, how epigenetic regulation contributes to this process remains unknown. We observed male-to-female sex reversal in mice lacking the H3K9 demethylase Jmjd1a and found that Jmjd1a regulates expression of the mammalian Y chromosome sex-determining gene Sry. Jmjd1a directly and positively controls Sry expression by regulating H3K9me2 marks. These studies reveal a pivotal role of histone demethylation in mammalian sex determination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuroki, Shunsuke -- Matoba, Shogo -- Akiyoshi, Mika -- Matsumura, Yasuko -- Miyachi, Hitoshi -- Mise, Nathan -- Abe, Kuniya -- Ogura, Atsuo -- Wilhelm, Dagmar -- Koopman, Peter -- Nozaki, Masami -- Kanai, Yoshiakira -- Shinkai, Yoichi -- Tachibana, Makoto -- New York, N.Y. -- Science. 2013 Sep 6;341(6150):1106-9. doi: 10.1126/science.1239864.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Research Center for Infectious Diseases, Institute for Virus Research, Kyoto University, 53 Shogoin, Kawara-cho, Sakyo-ku, Kyoto, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24009392" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Epididymis/abnormalities ; *Epigenesis, Genetic ; Female ; *Gene Expression Regulation, Developmental ; Histones/*metabolism ; Jumonji Domain-Containing Histone Demethylases/genetics/*metabolism ; Male ; Methylation ; Mice ; Mice, Mutant Strains ; Mice, Transgenic ; Ovary/abnormalities/enzymology ; *Protein Processing, Post-Translational ; Sex Determination Processes/*genetics ; Testis/abnormalities/enzymology ; Uterus/abnormalities
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
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    PAPER CURRENT
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