ArticleGene2018
Alternative splicing of (ppp1r12a/mypt1) in zebrafish produces a novel myosin phosphatase targeting subunit.
Article in Gene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed, 2 citations in OpenAlex.
- Clinical report and genetic analysis of a neonate with genitourinary and/or brain malformation syndrome caused by a non-coding sequence variant of PPP1R12A.Molecular genetics & genomic medicine · 2023Article
- The Evolution of Duplicated Genes of the Cpi-17/Phi-1 (International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Myosin phosphatase is an evolutionarily conserved regulator of actomyosin contractility, comprised of a regulatory subunit (Mypt1), and a catalytic subunit (PP1). Zebrafish has become an ideal model organism for the study of the genetic and cell physiological role of the myosin phosphatase in morphogenesis and embryonic development. We identified and characterized a novel splice variant of Mypt1 (ppp1r12a-tv202) from zebrafish, which is widely expressed during early embryonic development. Importantly, mutant alleles and antisense morpholinos that have been used to demonstrate the important role of Mypt1 in early development, not only disrupt the longer splice variants, but also tv202. The protein product of ppp1r12a-tv202 (Mypt1-202) contains the PP1-binding N-terminus, but lacks the regulatory C-terminus, which contains two highly conserved inhibitory phosphorylation sites. We observed that the protein product of tv202 assembled a constitutively active myosin phosphatase uninhibited by kinases such as Zipk. Thus, we propose that Mypt1-202 plays an important role in maintaining baseline Mlc2 dephosphorylation and actomyosin relaxation during early zebrafish development.
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Registered trials
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