ArticleThe EMBO journal2003
Hypomorphic mutation in an essential cell-cycle kinase causes growth retardation and impaired spermatogenesis.
Article in The EMBO journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 22 citations in OpenAlex.
- The structural basis of Cdc7-Dbf4 kinase dependent targeting and phosphorylation of the MCM2-7 double hexamer.Nature communications · 2022Article
- Genome-wide association study identifies 22 new loci for body dimension and body weight traits in a White Duroc×Erhualian FAsian-Australasian journal of animal sciences · 2017Article
- Transcriptome analysis reveals potential mechanisms underlying differential heart development in fast- and slow-growing broilers under heat stress.BMC genomics · 2017Article
- Self-organization of meiotic recombination initiation: general principles and molecular pathways.Annual review of genetics · 2014Review
- Cdc7-Dbf4 is a gene-specific regulator of meiotic transcription in yeast.Molecular and cellular biology · 2012Article
- Multiple pathways can bypass the essential role of fission yeast Hsk1 kinase in DNA replication initiation.The Journal of cell biology · 2011Article
- Cdc7-dependent phosphorylation of Mer2 facilitates initiation of yeast meiotic recombination.Genes & development · 2008Article
- Hsk1 kinase is required for induction of meiotic dsDNA breaks without involving checkpoint kinases in fission yeast.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cdc7 kinase is essential for initiation of DNA replication. Cdc7(-/-) mouse embryonic stem (ES) cells are non-viable but their growth can be rescued by an ectopically expressed transgene (Cdc7(-/-)tg). Here we report that, despite the normal growth capability of Cdc7(-/-)tg ES cells, the mice with the identical genetic background exhibit growth retardation. Concomi tantly, Cdc7(-/-)tg embryonic fibroblasts (MEFs) display delayed S phase entry and slow S phase progression. Furthermore, spermatogenesis of Cdc7(-/-)tg mice is disrupted prior to pachytene stage of meiotic prophase I. The impairment in spermatogenesis correlates with the extremely low level of Cdc7 protein in testes, and is rescued by introducing an additional allele of transgene, which results in increase of Cdc7 expression. The increased level of Cdc7 also recovers the growth of Cdc7(-/-)tg MEFs and mice, indicating that the developmental abnormalities of Cdc7(-/-)tg mice are due to insufficiency of Cdc7 protein. Our results indicate the requirement of a critical level of a cell-cycle regulator for mouse development and provide genetic evidence that Cdc7 plays essential roles in meiotic processes in mammals.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.