Disease relevance of myh10

• Despite the difference in normal growth-related hyperplasia in these fish, a vigorous regeneration occurred in both species, giving rise to new fibres with an initial myosin composition that differed from that in mature fast-white fibres [1].
• Importantly, altered expression of cardiac sarcomere components, including cardiac troponin T2 and multiple myosin isoforms, was consistent with the hypothesis that TCDD causes dilated cardiomyopathy [2].

High impact information on myh10

• A nonsense mutation in the gene encoding a zebrafish myosin VI isoform causes defects in hair-cell mechanotransduction [3].
• Mutation of weak atrium/atrial myosin heavy chain disrupts atrial function and influences ventricular morphogenesis in zebrafish [4].
• As weak atrium/atrial myosin heavy chain is expressed only in the atrium, the ventricular phenotypes in weak atrium mutants represent a secondary response to atrial dysfunction [4].
• Embryos with reduced myosin activity also exhibit at late stages of cytokinesis a stabilized contractile ring apparatus that appears as a ladder-like pattern of short f-actin cables, supporting a role for myosin function in the disassembly of the contractile ring after furrow formation [5].
• Our studies support a role for myosin function in furrow maturation that is independent of furrow ingression and which is essential for the recruitment of furrow components and the remodeling of the cytoskeleton during cytokinesis [5].

Biological context of myh10

• By using a fast and reproducible coinjection strategy, the mosaic expression of lacZ reporter gene was monitored in wholemount embryos injected with sequences containing putative enhancer elements and a carp myosin heavy chain promoter/lacZ reporter construct [6].
• In sea bream, myosin expression in regenerating fibres resembled that seen in new fibres produced in post-larval white muscle, whereas in the zebrafish it resembled that of the primitive monolayer fibres formed during embryonic development [1].
• Nuclear myosin I (NMI) is a single-headed member of myosin superfamily localized in the cell nucleus which participates along with nuclear actin in transcription and chromatin remodeling [7].

Anatomical context of myh10

• In the zebrafish, fibres of the slow twitch class arise from precociously specified myoblasts that lie close to the midline whereas the remainder of the myotome differentiates as fast myosin expressing muscle [8].
• We show that exposure to inhibitors of non-muscle myosin II function does not affect furrow ingression during the early cleavage cycles but interferes with the recruitment of pericleavage f-actin and cortical beta-catenin aggregates to the furrow, as well as the remodeling of the furrow microtubule array [5].
• The expression dynamics of myf5 in presomitic and somitic mesoderm suggest that RA promotes muscle differentiation, a role supported by the fact that RA activates expression of fast myosin, while DEAB represses it [9].
• Wortmannin induces zebrafish cardia bifida through a mechanism independent of phosphoinositide 3-kinase and myosin light chain kinase [10].
• Belbbistatin, a myosin II inhibitor, also caused blastomeres disintegration [11].

Associations of myh10 with chemical compounds

• Wortmannin has been reported to be a highly selective inhibitor of phosphoinositide 3-kinase and myosin light chain kinase activity [10].

Regulatory relationships of myh10

• We propose that polarized activation of the receptor CXCR4 leads to a rise in free calcium that in turn activates myosin contraction in the part of the cell responding to higher levels of the ligand SDF-1 [12].

Other interactions of myh10

• As an indicator of cardiac induction, we examine expression of nkx2.5, the earliest known marker of precardiac mesoderm; to assess anterior-posterior patterning, we distinguish ventricle from atrium with antibodies that recognize different myosin heavy chain isoforms [13].

References