|
職名 |
特命准教授 |
|
連絡先 |
|
|
外部リンク |
|
|
|
青木 敬太 (アオキ ケイタ) - 特命准教授 |
論文 【 表示 ／ 非表示 】
-
Malassezia display a hyphae-like “spaghetti and meatballs” configuration in keratotic plugs 査読あり
Otomi Cho, Mizuki Unno, Keita Aoki, Masako Takashima, Takashi Sugita
Medical Mycology Journal 2022年08月
記述言語：英語 掲載種別：研究論文（学術雑誌）
-
Atsushi T Onaka, Jie Su, Yasuhiro Katahira, Crystal Tang, Faria Zafar, Keita Aoki, Wataru Kagawa, Hironori Niki, Hiroshi Iwasaki, Takuro Nakagawa
Communications biology 3 ( 1 ) 202 - 202 2020年04月
記述言語：英語 掲載種別：研究論文（学術雑誌） 出版者・発行元：Springer Science and Business Media LLC
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.
-
Genetic defects in SAPK signalling, chromatin regulation, vesicle transport and CoA-related lipid metabolism are rescued by rapamycin in fission yeast 査読あり
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 8 ( 3 ) 2018年
記述言語：英語 掲載種別：研究論文（学術雑誌） 出版者・発行元：Royal Society Publishing
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： 10.1098/rsob.170261
-
Release of condensin from mitotic chromosomes requires the Ran-GTP gradient in the reorganized nucleus 査読あり
Keita Aoki, Hironori Niki
BIOLOGY OPEN 6 ( 11 ) 1614 - 1628 2017年11月
担当区分：筆頭著者 記述言語：英語 掲載種別：研究論文（学術雑誌） 出版者・発行元：COMPANY OF BIOLOGISTS LTD
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： 10.1242/bio.027193
-
Transformation of Schizosaccharomyces japonicus 査読あり
Aoki, K, Niki, H
Cold Spring Harbor Protocol doi: 10.1101/pdb.prot091850 2017年
担当区分：筆頭著者 記述言語：英語 掲載種別：研究論文（学術雑誌）
書籍等出版物 【 表示 ／ 非表示 】
-
染色体サイクル ゲノム恒常性維持、継承とダイナイクス内の概論「染色体の分配とM期制御」
青木敬太、仁木宏典（ 担当： 共著）
共立出版 2009年
記述言語：日本語 著書種別：学術書
科研費（文科省・学振）獲得実績 【 表示 ／ 非表示 】
-
新規モデル生物を用いた核膜動態の研究
2013年04月 - 2014年03月
科学研究費補助金 上原記念生命科学財団研究奨励金
青木敬太
講演・口頭発表等 【 表示 ／ 非表示 】
-
染色体脱凝縮に欠損を示すPim1/RCC1変異株の<em>Schizosaccharomyces japonicus</em>における解析
青木 敬太
第41回日本分子生物学会年会 2018年11月
開催年月日： 2018年11月
記述言語：日本語 会議種別：ポスター発表