FBS Colloquia No.160Laboratory of Stem Pathology
| Seminar or Lecture |
MIWI2 as an Effector of DNA Methylation and Gene Silencing in Embryonic Male Germ Cells Kanako Kita [Laboratory of Stem Cell Pathology] Transcripts selection as piRNA precursor Ippei Nagamori [Laboratory of Stem Cell Pathology] |
|---|---|
| Date and Time | Wednesday, May 17, 2017, 12:15-13:00 |
| Place | 2F Seminar room, BioSystems Building |
| Contact |
Shipnei Yamaguchi |
MIWI2 as an Effector of DNA Methylation and Gene Silencing in Embryonic Male Germ Cells
Small RNAs have critical roles for gene regulations and these abnormalities often lead to developmental arrest and/or diseases. Among small RNAs, we have focused on germ cell specific small RNA, named piRNA (PIWI-interacting RNA). piRNA functions as "genomic guardian" by repressing retrotransposon, and are essential for germ cell developments. Mouse piRNA binding protein, MILI (Mouse PIWI like) and MIWI2 (Mouse PIWI2) have crucial roles for piRNA biogenesis and its function, respectively. We have shown that majority of piRNA are derived from retrotransposons and they contributed for retrotransposon silencing by DNA methylation (Miyagawa et al 2008 Genes & Dev). Thus, physiological role of piRNA was reported almost 10 years ago, the molecular mechanisms remains elusive. In this seminar, we introduce recent findings in our lab "how MIWI2 complex induce piRNA-dependent DNA methylation", and "how piRNA-precursor transcripts are selected among a thousands of RNAs".
(Ref. Kita et al., 2016, Cell Rep.; Nagamori et al., 2015, Cell Rep.)
Transcripts selection as piRNA precursor
Small RNAs have critical roles for gene regulations and these abnormalities often lead to developmental arrest and/or diseases. Among small RNAs, we have focused on germ cell specific small RNA, named piRNA (PIWI-interacting RNA). piRNA functions as ""genomic guardian"" by repressing retrotransposon, and are essential for germ cell developments. Mouse piRNA binding protein, MILI (Mouse PIWI like) and MIWI2 (Mouse PIWI2) have crucial roles for piRNA biogenesis and its function, respectively. We have shown that majority of piRNA are derived from retrotransposons and they contributed for retrotransposon silencing by DNA methylation (Miyagawa et al 2008 Genes & Dev). Thus, physiological role of piRNA was reported almost 10 years ago, the molecular mechanisms remains elusive. In this seminar, we introduce recent findings in our lab "how MIWI2 complex induce piRNA-dependent DNA methylation", and "how piRNA-precursor transcripts are selected among a thousands of RNAs". (Ref. Kita et al., 2016, Cell Rep.; Nagamori et al., 2015, Cell Rep.)
