Disease relevance of sqh

• Planar polarization of the denticle field in the Drosophila embryo: Roles for Myosin II (Zipper) and Fringe [1].

High impact information on sqh

• The regulatory light chain of nonmuscle myosin is encoded by spaghetti-squash, a gene required for cytokinesis in Drosophila [2].
• Reversion by transposon excision or transformation with a wild-type copy of the sqh transcription unit rescues cytokinesis failure and other defects in sqh1 [2].
• Impairment of muscle function caused by mutations of phosphorylation sites in myosin regulatory light chain [3].
• Myosin regulatory light chain is phosphorylated by myosin light chain kinase at conserved serine and threonine residues in a number of species [3].
• We assessed the in vivo role of myosin regulatory light chain phosphorylation in the striated muscles of Drosophila melanogaster by substituting alanine at each or both conserved myosin light chain kinase-dependent phosphorylation sites, serine 66 and serine 67 [3].

Biological context of sqh

• Germ line cystoblasts entirely lacking a functional sqh gene show severe defects in proliferation and cytokinesis [4].
• Mutant sqh transgene sqh-A20, A21 in which both serine-21 and threonine-20 have been replaced by alanines behaves in most respects identically to the null allele in this system, with the exception that no heavy chain aggregates are found [4].
• This suggests that sqh mutant phenotypes are chiefly caused by sequestration of myosin into inactive aggregates [5].
• These findings suggest that increased levels of RLC phosphorylation do not contribute to disruption of the actomyosin hexagonal array [6].
• Although immunolocalization can only suggest possible function, these myosin localizations and the coincident changes in cell morphology are consistent with a key role for non-muscle myosin in powering cellularization and gastrulation during embryogenesis [7].

Anatomical context of sqh

• In addition, numerous aggregates of myosin heavy chain accumulate in the sqh null cells [4].
• Although activated PAK does not disrupt the actomyosin cytoskeleton, it induces increased levels of Ser21 phosphorylated RLC [6].
• At the syncytial blastoderm stage, myosin is found within cytoskeletal caps associated with the somatic nuclei at the embryonic surface [7].
• During cellularization, myosin is concentrated around the furrow canals that form the leading margin of the plasma membrane as it plunges inward to package each somatic nucleus into a columnar epithelial cell [7].
• In the preblastoderm embryo, myosin is localized to the egg cortex, sub-cortical arrays of inclusions, and, diffusely, the yolk-free periplasm [7].

Associations of sqh with chemical compounds

• Here we show that the S. pombe myosin light chain Cdc4p is phosphorylated in vivo on either serine 2 or 6 but not both [8].

Enzymatic interactions of sqh

• The I(20)/I(10) equatorial intensity ratio of the mutant fly is 35% less than that of wild type, supporting the hypothesis that myosin heads that lack phosphorylated RLC remain close to the thick filament backbone [9].

Regulatory relationships of sqh

• Vertebrate homologs of MRLC-C are phosphorylatable and regulate myosin activity in vitro [2].

Other interactions of sqh

• The Drosophila spaghetti squash (sqh) gene encodes the regulatory myosin light chain (RMLC) of nonmuscle myosin II [4].
• CONCLUSIONS/SIGNIFICANCE: We conclude that the Rho1 pathway leading to myosin localization to the future cytokinetic furrow is relatively straightforward, where only Rok is needed, and it is only needed to maintain phosphorylation of the myosin RLC [10].
• Furthermore, the essential role of Citron in cytokinesis is not phosphorylation of the RLC [10].
• Rho Kinase's Role in Myosin Recruitment to the Equatorial Cortex of Mitotic Drosophila S2 Cells Is for Myosin Regulatory Light Chain Phosphorylation [10].
• Mutations in myosin VIIA (myoVIIA), an unconventional myosin, lead to deafness and balance anomalies in humans, mice, and zebrafish; individuals are deaf, and stereocilia are disorganized [11].

Analytical, diagnostic and therapeutic context of sqh

• Although these regulators act to promote stable myosin accumulation and apical cell constriction, loss-of-function phenotypes for each of these pathway members is not equivalent, suggesting the existence of additional ventral furrow regulators [12].

References