ArticleFrontiers in oncology2012
Left-right symmetry breaking in mice by left-right dynein may occur via a biased chromatid segregation mechanism, without directly involving the Nodal gene.
Article in Frontiers in oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Biallelic loss of function NEK3 mutations deacetylate α-tubulin and downregulate NUP205 that predispose individuals to cilia-related abnormal cardiac left-right patterning.Cell death & disease · 2020Article
- Spiral waves and vertebrate embryonic handedness.Journal of biosciences · 2018Article
- Amar Klar: A giant among scientists (1947-2017).Journal of biosciences · 2017Article
- Stochastic left-right neuronal asymmetry in Caenorhabditis elegans.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016Review
- From cytoskeletal dynamics to organ asymmetry: a nonlinear, regulative pathway underlies left-right patterning.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016Review
- Split hand/foot malformation genetics supports the chromosome 7 copy segregation mechanism for human limb development.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016Review
- Diversity and convergence in the mechanisms establishing L/R asymmetry in metazoa.EMBO reports · 2014Review
- Selective chromatid segregation mechanism invoked for the human congenital mirror hand movement disorder development by RAD51 mutations: a hypothesis.International journal of biological sciences · 2014Review
- Long-range gap junctional signaling controls oncogene-mediated tumorigenesis in Xenopus laevis embryos.Frontiers in physiology · 2014Article
- Left-right patterning in Xenopus conjoined twin embryos requires serotonin signaling and gap junctions.The International journal of developmental biology · 2014Article
- Asymmetric cell division and template DNA co-segregation in cancer stem cells.Frontiers in oncology · 2014Review
- It's never too early to get it Right: A conserved role for the cytoskeleton in left-right asymmetry.Communicative & integrative biology · 2013Article
- A unified model for left-right asymmetry? Comparison and synthesis of molecular models of embryonic laterality.Developmental biology · 2013Review
- A CO-FISH assay to assess sister chromatid segregation patterns in mitosis of mouse embryonic stem cells.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2013Article
- Unbiased segregation of fission yeast chromosome 2 strands to daughter cells.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2013Review
- Implication of the Strand-Specific Imprinting and Segregation Model: IntegratingHereditary genetics : current research · 2013Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ever since cloning the classic iv (inversedviscerum) mutation identified the "left-right dynein" (lrd) gene in mice, most research on body laterality determination has focused on its function in motile cilia at the node embryonic organizer. This model is attractive, as it links chirality of cilia architecture to asymmetry development. However, lrd is also expressed in blastocysts and embryonic stem cells, where it was shown to bias the segregation of recombined sister chromatids away from each other in mitosis. These data suggested that lrd is part of a cellular mechanism that recognizes and selectively segregates sister chromatids based on their replication history: old "Watson" versus old "Crick" strands. We previously proposed that the mouse left-right axis is established via an asymmetric cell division prior to/or during gastrulation. In this model, left-right dynein selectively segregates epigenetically differentiated sister chromatids harboring a hypothetical "left-right axis development 1" ("lra1") gene during the left-right axis establishing cell division. Here, asymmetry development would be ultimately governed by the chirality of the cytoskeleton and the DNA molecule. Our model predicts that randomization of chromatid segregation in lrd mutants should produce embryos with 25% situs solitus, 25% situs inversus, and 50% embryonic death due to heterotaxia and isomerism. Here we confirmed this prediction by using two distinct lrd mutant alleles. Other than lrd, thus far Nodal gene is the most upstream function implicated in visceral organs laterality determination. We next tested whether the Nodal gene constitutes the lra1 gene hypothesized in the model by testing mutant's effect on 50% embryonic lethality observed in lrd mutants. Since Nodal mutation did not suppress lethality, we conclude that Nodal is not equivalent to the lra1 gene. In summary, we describe the origin of 50% lethality in lrd mutant mice not yet explained by any other laterality-generating hypothesis.
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