ArticleMolecular and cellular biology2004
The ubiquitin-conjugating DNA repair enzyme HR6A is a maternal factor essential for early embryonic development in mice.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
55 citing papers in PubMed, 113 citations in OpenAlex.
- Maternal PRDM10 activates essential genes for oocyte-to-embryo transition.Nature communications · 2025Article
- Selective Translation of Maternal mRNA by eIF4E1B Controls Oocyte to Embryo Transition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Genetic basis of maize maternal haploid induction beyondFrontiers in plant science · 2023Article
- Maternal effect factors that contribute to oocytes developmental competence: an update.Journal of assisted reproduction and genetics · 2022Review
- The neglected part of early embryonic development: maternal protein degradation.Cellular and molecular life sciences : CMLS · 2020Review
- Maternal factors regulating preimplantation development in mice.Current topics in developmental biology · 2020Review
- Perturbation of maternal PIASy abundance disrupts zygotic genome activation and embryonic development via SUMOylation pathway.Biology open · 2019Article
- Article
- DNA damage tolerance in stem cells, ageing, mutagenesis, disease and cancer therapy.Nucleic acids research · 2019Review
- Histone H2B monoubiquitination regulates heart development via epigenetic control of cilia motility.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Dynamics of the epigenetic landscape during the maternal-to-zygotic transition.Nature reviews. Molecular cell biology · 2018Review
- FANCD2 and DNA Damage.International journal of molecular sciences · 2017Review
- Involvement of FANCD2 in Energy Metabolism via ATP5α.Scientific reports · 2017Article
- Pharmacological targeting of RAD6 enzyme-mediated translesion synthesis overcomes resistance to platinum-based drugs.The Journal of biological chemistry · 2017Article
- In vitro developmental ability of ovine oocytes following intracytoplasmic injection with freeze-dried spermatozoa.Scientific reports · 2017Article
- Overlooked FANCD2 variant encodes a promising, portent tumor suppressor, and alternative polyadenylation contributes to its expression.Oncotarget · 2017Article
- The miR-125 family is an important regulator of the expression and maintenance of maternal effect genes during preimplantational embryo development.Open biology · 2016Article
- The Role of Maternal-Effect Genes in Mammalian Development: Are Mammalian Embryos Really an Exception?Stem cell reviews and reports · 2016Review
- Loss of the Ubiquitin-conjugating Enzyme UBE2W Results in Susceptibility to Early Postnatal Lethality and Defects in Skin, Immune, and Male Reproductive Systems.The Journal of biological chemistry · 2016Article
- Chromosomal instability in mammalian pre-implantation embryos: potential causes, detection methods, and clinical consequences.Cell and tissue research · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Saccharomyces cerevisiae RAD6 protein is required for a surprising diversity of cellular processes, including sporulation and replicational damage bypass of DNA lesions. In mammals, two RAD6-related genes, HR6A and HR6B, encode highly homologous proteins. Here, we describe the phenotype of cells and mice deficient for the mHR6A gene. Just like mHR6B knockout mouse embryonic fibroblasts, mHR6A-deficient cells appear to have normal DNA damage resistance properties, but mHR6A knockout male and female mice display a small decrease in body weight. The necessity for at least one functional mHR6A (X-chromosomal) or mHR6B (autosomal) allele in all somatic cell types is supported by the fact that neither animals lacking both proteins nor females with only one intact mHR6A allele are viable. In striking contrast to mHR6B knockout males, which show a severe spermatogenic defect, mHR6A knockout males are normally fertile. However, mHR6A knockout females fail to produce offspring despite a normal ovarian histology and ovulation. The absence of mHR6A in oocytes prevents development beyond the embryonic two-cell stage but does not result in an aberrant methylation pattern of histone H3 at this early stage of mouse embryonic development. These observations support redundant but dose-dependent roles for HR6A and HR6B in somatic cell types and germ line cells in mammals.
Indexed as
Identifiers
What OpenQuestion holds
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.