Earticle

초록

영어

Meiotic oocytes lack classic centrosomes; therefore, bipolar-spindle assembly depends on the clustering of acentriolar microtubule-organizing centers (MTOCs) into two poles. Tumor suppressor P53-binding protein 1 (TP53BP1) is a known mediator in DNA damage response. Recent studies have revealed a new role of TP53BP1 in maintaining centrosome integrity in mitosis. However, the role of TP53BP1 in oocyte meiosis is unclear. Our results show that TP53BP1 participates in DNA damage responses in oocyte, as well as stablishment of chromosome alignment and spindle bipolarity by controlling the clustering of MTOCs during oocyte maturation. TP53BP1 was localized in the cytoplasm and concentrated around the spindle/chromosome region. Knockdown of TP53BP1 induced abnormal DNA damage response involving RAD51 and formation of γH2AX foci. TP53BP1 was also required for the clustering of MTOCs into two spindle poles during pro-meiosis I. Deletion of TP53BP1 induced perturbation in MTOC-localized Aurora Kinase A (AURKA). The knockdown of TP53BP1 induced microtubules to dis-attach from the kinetochores and increased the rate of aneuploidy. Taken together, our data show that TP53BP1 plays crucial roles in chromosome stability and spindle bipolarity during meiotic maturation by regulating the clustering of MTOCs.

키워드

저자

• Zhe-Long Jin [ Department of Animal Sciences, Chungbuk National University ]
• Suk Namgoong [ Department of Animal Sciences, Chungbuk National University ]
• Nam-Hyung Kim [ Department of Animal Sciences, Chungbuk National University ]

참고문헌

발행기관

간행물

표지보기 관심저널 등록

• 간행물명

  발생공학 국제심포지엄 및 학술대회 [International Symposium on Developmental Biotechnology]

• 간기

  연간

• 수록기간

  2004~2018

• 십진분류

  KDC 527 DDC 636