オカモト　カズコ   Kazuko Okamoto   岡本　和子    所属   川崎医科大学  医学部 一般教養　自然科学    職種   助教
論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	Effect of Cdk1 gene disruption on cell cycle progression in newt cells.
掲載誌名	正式名：Development, growth & differentiation 略　 称：Dev Growth Differ ISSNコード：1440169X/00121592
掲載区分	国外
巻・号・頁	67(2),pp.85-93
著者・共著者	Yuta Nakao, Kazuko Okamoto, Ichiro Tazawa, Tatsuro Nishijima, Nobuaki Furuno, Tetsushi Sakuma, Takashi Yamamoto, Takashi Takeuchi, Toshinori Hayashi
担当区分	2nd著者
発行年月	2025/02
概要	Cyclin-dependent kinases (CDKs) are key regulators of cell cycle progression, in conjunction with cyclins. The cyclin-CDK system is highly conserved among eukaryotes, and CDK1 is considered essential for progression through the M phase. However, the extent to which cell cycle progression depends on CDK1 varies between cell types. Therefore, a range of cell types must be analyzed to comprehensively elucidate the role of CDK1. Cdk1-knockout mice exhibit lethality at an early developmental stage, specifically before the differentiation of various cell types. The aim of the present study was to characterize the effects of CDK1 deficiency in amphibian newts. Cdk1 was disrupted by injecting fertilized newt eggs with CRISPR/Cas9, and the resulting effects on embryonic development and cell proliferation were then evaluated. In both wild-type and Cdk1-crispant newt embryos, CDK1 protein was either stored in the egg until late embryogenesis or potentially derived from maternal mRNA, which may also be stored during this period. The embryos survived to the hatching stage, during which the cells responsible for forming the basic organs differentiated. To further characterize the long-term effects of Cdk1 knockout, parabiosis experiments were conducted using wild-type embryos and Cdk1 crispants. The results suggested that an endocycle occurred in the crispant larvae, as evidenced by increases in the size of several types of cells. It is anticipated that studies using newts will provide further insights into the role of Cdk1 in regulating the cell cycle.
DOI	10.1111/dgd.12958
PMID	39776058