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Gene Review

Myl1  -  myosin, light polypeptide 1

Mus musculus

Synonyms: AI325107, MLC1/MLC3, MLC1F/MLC3F, MLC1f, MLC3f, ...
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Disease relevance of Myl1


High impact information on Myl1

  • Two loci have been characterized in the mouse Mus musculus, which are homologous to the mRNAs encoding myosin light chains MLC1F and MLC3F, two proteins with a common -COOH terminal sequence [6].
  • Genetic information specific for the N-terminal sequences is encoded in four exons, at 3.5 and 14.3 kb for MLC1F, and 3.8 and 4.5 kb for MLC3F, upstream of the first common exon [6].
  • The pseudogene is not genetically linked to the functional MLC1F/MLC3F locus in the genome of Mus musculus [6].
  • One of these loci is an intronless pseudogene, absent from the mouse species Mus spretus; alterations in its nucleotide sequence preclude it from generating a functional MLC1F or MLC3F [6].
  • Homozygous mutants had no circulating or atrial ANP, and their blood pressures were elevated by 8 to 23 millimeters of mercury when they were fed standard (0.5 percent sodium chloride) and intermediate (2 percent sodium chloride) salt diets [7].

Chemical compound and disease context of Myl1

  • Expression of extracellular ligand-binding domain of murine guanylate cyclase/atrial natriuretic factor receptor cDNA in Escherichia coli [8].
  • Recent studies have suggested that inositol-1,4,5-trisphosphate-receptor (IP3R)-mediated Ca2+ release plays an important role in the modulation of excitation-contraction coupling (ECC) in atrial tissue and the generation of arrhythmias, specifically chronic atrial fibrillation (AF) [9].
  • Mice made obese with gold thioglucose developed cardiac hypertrophy associated with increases in ANP in atrial tissue and plasma [10].
  • Since a bovine brain ganglioside mixture (Cronassial) has been extensively studied for its effect on peripheral diabetic neuropathy, a group of diabetic mice was treated throughout the sixth month with this drug (10 mg/kg/day i.p.). The ganglioside treated animals showed a marked recovery of atrial function and cardiac NE concentration [11].

Biological context of Myl1


Anatomical context of Myl1


Associations of Myl1 with chemical compounds

  • The NH2-terminal region of MLC1A/MLC1emb, thought to be involved in the actomyosin interaction, shows conservation with MLC1V but not with MLC1F suggesting a shared functional domain in these cardiac isoforms [19].
  • Effect of native and synthetic atrial natriuretic factor on cyclic GMP [20].
  • Reduced plasma epinephrine and corticosterone levels and adrenal medullary EGR-1 protein levels in CRH knockout versus WT mice during stress indicate that the HPA axis plays a crucial role in regulation of the PNMT gene expression in these organs.Cardiac atrial PNMT gene expression with stress is also dependent on intact HPA axis [21].
  • 3. Mean arterial pressure and atrial, LV and RV mass were greater in ANP-/- mice than in ANP+/+ mice fed the basal salt diet [22].
  • We confirm this intracaveolar localization by stereoimaging colloidal gold-labeled antibody to the prohormone in electron micrographs of glutaraldehyde/osmium tetroxide-fixed positively stained atrial thin sections [23].

Physical interactions of Myl1

  • The membrane-bound form of guanylate cyclase/atrial natriuretic factor receptor (GC/ANF-R) is a 135 kDa transmembrane glycoprotein which binds ANF with high affinity [8].

Regulatory relationships of Myl1

  • Furthermore, during the course of ANF purification, the ANF-induced increase of cGMP production by kidney cells paralleled the heightened specific natriuretic activity of the atrial factor [20].
  • However, GLUT4 but not vp165 is additionally localised in the regulated secretory pathway in atrial cardiomyocytes [24].
  • Endothelin-1-induced arrhythmogenic Ca2+ signaling is abolished in atrial myocytes of inositol-1,4,5-trisphosphate(IP3)-receptor type 2-deficient mice [9].
  • 1. Peak outward K+ current densities are attenuated significantly in atrial myocytes isolated from P15 and adult Kv2.1N216Flag-expressing animals and in P15 cells exposed to AsODNs targeted against either Kv1.5 or Kv2 [25].
  • Phospholamban gene transcript levels are much lower in murine atria as compared to murine ventricles and this reduced phospholamban expression has been suggested to result in enhanced atrial contractile parameters [26].

Other interactions of Myl1

  • In contrast, the cardiac MLC1A mRNA is initially more abundant than that encoding the skeletal MLC1F isoform [13].
  • However, although left-sided identity is later maintained by Pitx2 genes, we found that Pitx2c null embryos have normal left-biased expression of alpha-skeletal actin and MLC3F [1].
  • An additional 47 backcross progeny from a cross between C57BL/10ScSn and B10.L-Lshr/s mice were examined for the cosegregation of Myl-1 and Vil RFLPs with Lsh phenotypic differences [27].
  • Changes in atrial volume and ECF translocation and ANP secretion were positively correlated [17].
  • The rostrocaudal positional gradient of transgene expression documented for MLC1F transgenic mice (Donoghue, M., J. P. Merlie, N. Rosenthal, and J. R. Sanes. 1991. Proc. Natl. Acad. Sci. USA. 88:5847-5851) is not seen in MLC3F transgenic mice [12].

Analytical, diagnostic and therapeutic context of Myl1


  1. Mouse myotomes pairs exhibit left-right asymmetric expression of MLC3F and alpha-skeletal actin. Golding, J.P., Partridge, T.A., Beauchamp, J.R., King, T., Brown, N.A., Gassmann, M., Zammit, P.S. Dev. Dyn. (2004) [Pubmed]
  2. Fine-tuning of cross-bridge kinetics in cardiac muscle of rat and mouse by myosin light chain isoforms. Andruchov, O., Andruchova, O., Galler, S. Pflugers Arch. (2006) [Pubmed]
  3. Molecular and physiological alterations in murine ventricular dysfunction. Rockman, H.A., Ono, S., Ross, R.S., Jones, L.R., Karimi, M., Bhargava, V., Ross, J., Chien, K.R. Proc. Natl. Acad. Sci. U.S.A. (1994) [Pubmed]
  4. Hypoxia stimulates atrial natriuretic peptide gene expression in cultured atrial cardiocytes. Chen, Y.F., Durand, J., Claycomb, W.C. Hypertension (1997) [Pubmed]
  5. Activation of the gene for atrial natriuretic factor during in vitro cardiac myogenesis by P19 embryonal carcinoma cells. Boer, P.H. Exp. Cell Res. (1993) [Pubmed]
  6. A single locus in the mouse encodes both myosin light chains 1 and 3, a second locus corresponds to a related pseudogene. Robert, B., Daubas, P., Akimenko, M.A., Cohen, A., Garner, I., Guenet, J.L., Buckingham, M. Cell (1984) [Pubmed]
  7. Genetic decreases in atrial natriuretic peptide and salt-sensitive hypertension. John, S.W., Krege, J.H., Oliver, P.M., Hagaman, J.R., Hodgin, J.B., Pang, S.C., Flynn, T.G., Smithies, O. Science (1995) [Pubmed]
  8. Expression of extracellular ligand-binding domain of murine guanylate cyclase/atrial natriuretic factor receptor cDNA in Escherichia coli. Pandey, K.N., Kanungo, J. Biochem. Biophys. Res. Commun. (1993) [Pubmed]
  9. Endothelin-1-induced arrhythmogenic Ca2+ signaling is abolished in atrial myocytes of inositol-1,4,5-trisphosphate(IP3)-receptor type 2-deficient mice. Li, X., Zima, A.V., Sheikh, F., Blatter, L.A., Chen, J. Circ. Res. (2005) [Pubmed]
  10. Cardiac atrial natriuretic peptide concentrations in experimental obese mice. Iida, T., Hirata, Y., Takahashi, H., Ikeda, K., Nakagawa, S. Endocrinol. Jpn. (1990) [Pubmed]
  11. Effects of long-term diabetes and treatment with gangliosides on cardiac sympathetic innervation: a biochemical and functional study in mice. Tessari, F., Travagli, R.A., Zanoni, R., Prosdocimi, M. The Journal of diabetic complications. (1988) [Pubmed]
  12. Myosin light chain 3F regulatory sequences confer regionalized cardiac and skeletal muscle expression in transgenic mice. Kelly, R., Alonso, S., Tajbakhsh, S., Cossu, G., Buckingham, M. J. Cell Biol. (1995) [Pubmed]
  13. The expression of myosin genes in developing skeletal muscle in the mouse embryo. Lyons, G.E., Ontell, M., Cox, R., Sassoon, D., Buckingham, M. J. Cell Biol. (1990) [Pubmed]
  14. Myosin light chain gene expression in developing and denervated fetal muscle in the mouse. Barton, P.J., Harris, A.J., Buckingham, M.E. Development (1989) [Pubmed]
  15. Contractile protein gene expression in primary myotubes of embryonic mouse hindlimb muscles. Ontell, M., Ontell, M.P., Sopper, M.M., Mallonga, R., Lyons, G., Buckingham, M. Development (1993) [Pubmed]
  16. Dynamic left/right regionalisation of endogenous myosin light chain 3F transcripts in the developing mouse heart. Kelly, R.G., Zammit, P.S., Mouly, V., Butler-Browne, G., Buckingham, M.E. J. Mol. Cell. Cardiol. (1998) [Pubmed]
  17. Stretch-activated atrial natriuretic peptide secretion in atria with heat shock protein 70 overexpression. Kim, S.H., Koh, G.Y., Cho, K.W., Park, W.Y., Seo, J.S. Exp. Biol. Med. (Maywood) (2003) [Pubmed]
  18. Embryonic and fetal myogenic programs act through separate enhancers at the MLC1F/3F locus. Kelly, R.G., Zammit, P.S., Schneider, A., Alonso, S., Biben, C., Buckingham, M.E. Dev. Biol. (1997) [Pubmed]
  19. Structure and sequence of the myosin alkali light chain gene expressed in adult cardiac atria and fetal striated muscle. Barton, P.J., Robert, B., Cohen, A., Garner, I., Sassoon, D., Weydert, A., Buckingham, M.E. J. Biol. Chem. (1988) [Pubmed]
  20. Effect of native and synthetic atrial natriuretic factor on cyclic GMP. Hamet, P., Tremblay, J., Pang, S.C., Garcia, R., Thibault, G., Gutkowska, J., Cantin, M., Genest, J. Biochem. Biophys. Res. Commun. (1984) [Pubmed]
  21. Gene expression of phenylethanolamine N-methyltransferase in corticotropin-releasing hormone knockout mice during stress exposure. Kvetnansky, R., Kubovcakova, L., Tillinger, A., Micutkova, L., Krizanova, O., Sabban, E.L. Cell. Mol. Neurobiol. (2006) [Pubmed]
  22. Pressure-independent enhancement of cardiac hypertrophy in atrial natriuretic peptide-deficient mice. Feng, J.A., Perry, G., Mori, T., Hayashi, T., Oparil, S., Chen, Y.F. Clin. Exp. Pharmacol. Physiol. (2003) [Pubmed]
  23. Localization of atrial natriuretic peptide in caveolae of in situ atrial myocytes. Page, E., Upshaw-Earley, J., Goings, G.E. Circ. Res. (1994) [Pubmed]
  24. The glucose transporter GLUT4 and the aminopeptidase vp165 colocalise in tubulo-vesicular elements in adipocytes and cardiomyocytes. Martin, S., Rice, J.E., Gould, G.W., Keller, S.R., Slot, J.W., James, D.E. J. Cell. Sci. (1997) [Pubmed]
  25. Molecular diversity of the repolarizing voltage-gated K+ currents in mouse atrial cells. Bou-Abboud, E., Li, H., Nerbonne, J.M. J. Physiol. (Lond.) (2000) [Pubmed]
  26. Phospholamban modulates murine atrial contractile parameters and responses to beta-adrenergic agonists. Kadambi, V.J., Koss, K.L., Grupp, I.L., Kranias, E.G. J. Mol. Cell. Cardiol. (1998) [Pubmed]
  27. A genetic map of mouse chromosome 1 near the Lsh-Ity-Bcg disease resistance locus. Mock, B., Krall, M., Blackwell, J., O'Brien, A., Schurr, E., Gros, P., Skamene, E., Potter, M. Genomics (1990) [Pubmed]
  28. Positional specification of ventricular myosin light chain 2 expression in the primitive murine heart tube. O'Brien, T.X., Lee, K.J., Chien, K.R. Proc. Natl. Acad. Sci. U.S.A. (1993) [Pubmed]
  29. Three-dimensional MR microscopy of a transgenic mouse model of dilated cardiomyopathy. Sze, R.W., Chan, C.B., Dardzinski, B.J., Dunn, S., Sanbe, A., Schmithorst, V., Robbins, J., Holland, S.K., Strife, J.L. Pediatric radiology. (2001) [Pubmed]
  30. Kir6.2-deficient mice are susceptible to stimulated ANP secretion: K(ATP) channel acts as a negative feedback mechanism? Saegusa, N., Sato, T., Saito, T., Tamagawa, M., Komuro, I., Nakaya, H. Cardiovasc. Res. (2005) [Pubmed]
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