2022/05/06 更新

写真b

青木 敬太 (アオキ ケイタ)

-

特命准教授

メールアドレス

メールアドレス

学内職務経歴 【 表示 / 非表示

  • 2022年04月
    -
    継続中

    東京農業大学   総合研究所   特命准教授  

論文 【 表示 / 非表示

  • Malassezia display a hyphae-like “spaghetti and meatballs” configuration in keratotic plugs

    Otomi Cho, Mizuki Unno, Keita Aoki, Masako Takashima, Takashi Sugita

    Medical Mycology Journal     2022年08月  [査読有り]

    研究論文(学術雑誌)   共著

  • DNA replication machinery prevents Rad52-dependent single-strand annealing that leads to gross chromosomal rearrangements at centromeres.

    Atsushi T Onaka, Jie Su, Yasuhiro Katahira, Crystal Tang, Faria Zafar, Keita Aoki, Wataru Kagawa, Hironori Niki, Hiroshi Iwasaki, Takuro Nakagawa

    Communications biology ( Springer Science and Business Media LLC )  3 ( 1 ) 202 - 202   2020年04月  [査読有り]

    研究論文(学術雑誌)   共著

    Homologous recombination between repetitive sequences can lead to gross chromosomal rearrangements (GCRs). At fission yeast centromeres, Rad51-dependent conservative recombination predominantly occurs between inverted repeats, thereby suppressing formation of isochromosomes whose arms are mirror images. However, it is unclear how GCRs occur in the absence of Rad51 and how GCRs are prevented at centromeres. Here, we show that homology-mediated GCRs occur through Rad52-dependent single-strand annealing (SSA). The rad52-R45K mutation, which impairs SSA activity of Rad52 protein, dramatically reduces isochromosome formation in rad51 deletion cells. A ring-like complex Msh2-Msh3 and a structure-specific endonuclease Mus81 function in the Rad52-dependent GCR pathway. Remarkably, mutations in replication fork components, including DNA polymerase α and Swi1/Tof1/Timeless, change the balance between Rad51-dependent recombination and Rad52-dependent SSA at centromeres, increasing Rad52-dependent SSA that forms isochromosomes. Our results uncover a role of DNA replication machinery in the recombination pathway choice that prevents Rad52-dependent GCRs at centromeres.

    DOI PubMed

  • Genetic defects in SAPK signalling, chromatin regulation, vesicle transport and CoA-related lipid metabolism are rescued by rapamycin in fission yeast

    Kenichi Sajiki, Yuria Tahara, Alejandro Villar-Briones, Tomáš Pluskal, Takayuki Teruya, Ayaka Mori, Mitsuko Hatanaka, Masahiro Ebe, Takahiro Nakamura, Keita Aoki, Yukinobu Nakaseko, Mitsuhiro Yanagida

    Open Biology ( Royal Society Publishing )  8 ( 3 )   2018年  [査読有り]

    研究論文(学術雑誌)   共著

    Rapamycin inhibits TOR (target of rapamycin) kinase, and is being used clinically to treat various diseases ranging from cancers to fibrodysplasia ossificans progressiva. To understand rapamycin mechanisms of action more comprehensively, 1014 temperature-sensitive (ts) fission yeast (Schizosaccharomyces pombe) mutants were screened in order to isolate strains in which the ts phenotype was rescued by rapamycin. Rapamycin-rescued 45 strains, among which 12 genes responsible for temperature sensitivity were identified. These genes are involved in stress-activated protein kinase (SAPK) signalling, chromatin regulation, vesicle transport, and CoA- and mevalonate-related lipid metabolism. Subsequent metabolome analyses revealed that rapamycin upregulated stress-responsive metabolites, while it downregulated purine biosynthesis intermediates and nucleotide derivatives. Rapamycin alleviated abnormalities in cell growth and cell division caused by sty1 mutants (Dsty1) of SAPK. Notably, in Dsty1, rapamycin reduced greater than 75% of overproduced metabolites (greater than 2 WT), like purine biosynthesis intermediates and nucleotide derivatives, to WT levels. This suggests that these compounds May be the points at which the SAPK/TOR balance regulates continuous cell proliferation. Rapamycin might be therapeutically useful for specific defects of these gene functions.

    DOI

  • Release of condensin from mitotic chromosomes requires the Ran-GTP gradient in the reorganized nucleus

    Keita Aoki, Hironori Niki

    BIOLOGY OPEN ( COMPANY OF BIOLOGISTS LTD )  6 ( 11 ) 1614 - 1628   2017年11月  [査読有り]

    研究論文(学術雑誌)   共著

    After mitosis, nuclear reorganization occurs together with decondensation of mitotic chromosomes and reformation of the nuclear envelope, thereby restoring the Ran-GTP gradient between the nucleus and cytoplasm. The Ran-GTP gradient is dependent on Pim1/RCC1. Interestingly, a defect in Pim1/RCC1 in Schizosaccharomyces pombe causes postmitotic condensation of chromatin, namely hypercondensation, suggesting a relationship between the Ran-GTP gradient and chromosome decondensation. However, how Ran-GTP interacts with chromosome decondensation is unresolved. To examine this interaction, we used Schizosaccharomyces japonicus, which is known to undergo partial breakdown of the nuclear membrane during mitosis. We found that Pim1/RCC1 was localized on nuclear pores, but this localization failed in a temperature-sensitive mutant of Pim1/RCC1. The mutant cells exhibited hypercondensed chromatin after mitosis due to prolonged association of condensin on the chromosomes. Conceivably, a condensin-dephosphorylation defect might cause hypercondensed chromatin, since chromosomal localization of condensin is dependent on phosphorylation by cyclin-dependent kinase (CDK). Indeed, CDK-phospho-mimic mutation of condensin alone caused untimely condensin localization, resulting in hypercondensed chromatin. Together, these results suggest that dephosphorylation of CDK sites of condensin might require the Ran-GTP gradient produced by nuclear pore-localized Pim1/RCC1.

    DOI

  • Transformation of Schizosaccharomyces japonicus

    Aoki, K, Niki, H

    Cold Spring Harbor Protocol   doi: 10.1101/pdb.prot091850   2017年  [査読有り]

    研究論文(学術雑誌)   共著

全件表示 >>

研究発表 【 表示 / 非表示