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Associate Professor, UC Department of Pediatrics
Dr. Namekawa received his PhD from Tokyo University of Science in 2005. He completed postdoctoral training in the laboratory of Dr. Jeannie T. Lee at Massachusetts General Hospital and Harvard Medical School in 2009, and attained his faculty appointment at Cincinnati Children's Hospital Medical Center in 2009. He received the Basil O’Connor Award from March of Dimes Foundation in 2011, the New Investigator Award from the Society for the Study of Reproduction in 2015, and the Research Achievement Award from Cincinnati Children’s Hospital Medical Center in 2016.
The long-term goal of the Namekawa laboratory is to reveal and fully explain epigenetic mechanisms in germ cells and stem cells, with an emphasis on how germline identity is defined and the recovery of totipotency after fertilization—mechanisms that are ultimately responsible for the perpetuity of life. Specifically, the laboratory focuses on how the epigenome is preset, or poised, in stem cells for gene regulation in subsequent stages of differentiating germ cells, thereby ensuring stage-specific transcriptional regulation in the context of germ cell development and aging. Illumination of these mechanisms will explain the central identity of the germline and address how epigenetic information is transmitted across generations. Further, the laboratory aims to identify mechanisms by which the integrity of the germline is ensured, as this is key to understanding how the integrity of life is ensured, an essential and longstanding question in biology. Another area of focus is the epigenetic regulation of sex chromosomes in germ cell development, with an emphasis on how the sex chromosomes specifically function for reproduction.
Reproductive Sciences, Developmental Biology
Satoshi H. Namekawa, PhD9/7/2020
Satoshi H. Namekawa, PhD7/3/2019
PhD: Tokyo University of Science, Japan, 2005.
BS: Tokyo University of Science, Japan, 2000.
FANCD2 is required for the repression of germline transposable elements.
Nie, Y; Wilson, AF; DeFalco, T; Meetei, AR; Namekawa, SH; Pang, Q.
Pioneering meiotic recombination.
Alavattam, KG; Abe, H; Namekawa, SH.
Genes and Development.
The Initiation of Meiotic Sex Chromosome Inactivation Sequesters DNA Damage Signaling from Autosomes in Mouse Spermatogenesis.
Abe, H; Alavattam, KG; Hu, Y; Pang, Q; Andreassen, PR; Hegde, RS; Namekawa, SH.
UHRF1 suppresses retrotransposons and cooperates with PRMT5 and PIWI proteins in male germ cells.
Dong, J; Wang, X; Cao, C; Wen, Y; Sakashita, A; Chen, S; Zhang, J; Zhang, Y; Zhou, L; Luo, M; et al.
Attenuated chromatin compartmentalization in meiosis and its maturation in sperm development.
Alavattam, KG; Maezawa, S; Sakashita, A; Khoury, H; Barski, A; Kaplan, N; Namekawa, SH.
Nature Structural and Molecular Biology.
XY oocytes of sex-reversed females with a Sry mutation deviate from the normal developmental process beyond the mitotic stage.
Sakashita, A; Wakai, T; Kawabata, Y; Nishimura, C; Sotomaru, Y; Alavattam, KG; Namekawa, SH; Kono, T.
Biology of Reproduction.
A rapidly evolved domain, the SCML2 DNA-binding repeats, contributes to chromatin binding of mouse SCML2.
Maezawa, S; Alavattam, KG; Tatara, M; Nagai, R; Barski, A; Namekawa, SH.
Biology of Reproduction.
SCML2 promotes heterochromatin organization in late spermatogenesis.
Maezawa, S; Hasegawa, K; Alavattam, KG; Funakoshi, M; Sato, T; Barski, A; Namekawa, SH.
Journal of Cell Science.
Polycomb protein SCML2 facilitates H3K27me3 to establish bivalent domains in the male germline.
Maezawa, S; Hasegawa, K; Yukawa, M; Kubo, N; Sakashita, A; Alavattam, KG; Sin, H; Kartashov, AV; Sasaki, H; Barski, A; et al.
Proceedings of the National Academy of Sciences of USA.
CHEK1 coordinates DNA damage signaling and meiotic progression in the male germline of mice.
Abe, H; Alavattam, KG; Kato, Y; Castrillon, DH; Pang, Q; Andreassen, PR; Namekawa, SH.
Human Molecular Genetics.
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