PUBLICATION
Loss-of-function of zebrafish cdt1 causes retarded body growth and underdeveloped gonads resembling human Meier-Gorlin syndrome
- Authors
- He, Y., Wang, Y., Zhu, Y., Lo, L.J.
- ID
- ZDB-PUB-231114-23
- Date
- 2023
- Source
- Journal of Zhejiang University. Science. B 24: 103710461037-1046 (Journal)
- Registered Authors
- Li Jan, Lo
- Keywords
- none
- MeSH Terms
-
- Animals
- Cell Cycle Proteins
- Gonads
- Growth Disorders*
- Humans
- Zebrafish*
- PubMed
- 37961805 Full text @ J. Zhejiang Univ. Sci. B
Citation
He, Y., Wang, Y., Zhu, Y., Lo, L.J. (2023) Loss-of-function of zebrafish cdt1 causes retarded body growth and underdeveloped gonads resembling human Meier-Gorlin syndrome. Journal of Zhejiang University. Science. B. 24:103710461037-1046.
Abstract
The cell cycle consists of four distinct phases: G0/G1, S (DNA synthesis), G2, and M (mitosis). The G1 to S transition is typified by an accumulation of 4',?6-diamidino-2-phenylindole (DAPI) signal that indicates the rapid DNA synthesis initiated at special sites on DNA, generally called the Ori (origin of replication) (Alfa et al., 1989). The cell division cycle 10 (Cdc10)?-dependent transcript 1 (Cdt1) is bestowed the term �replication origin licensing factor� for its role in warranting replication once (and only once) per round of the eukaryotic cell cycle, during the S phase (Pozo and Cook, 2017). In a normal cell cycle, Cdt1 is present only in the G1 and S entry phases, whereas Geminin, a protein that targets Cdt1 for S-phase-dependent proteolysis, is present in the S and G2 phases. Failure of this gatekeeping task as observed in cdt1 overexpression, for example in yeast, leads to inappropriate origin firing (also termed re-replication (Vaziri et al., 2003)) and eventually DNA damage checkpoint activation (Kanellou et al., 2020).
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping