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Gene Review

Myl3  -  myosin, light polypeptide 3

Mus musculus

Synonyms: MLC1SB, MLC1s, MLC1v, Mlc1v, Mylc, ...
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Disease relevance of Myl3

  • To determine if activation of ras-dependent intracellular signaling pathways is sufficient to induce in vivo hypertrophy, transgenic mice were created that express oncogenic ras in the cardiac ventricular chamber [1].
  • However, despite the substitution of myosin light chain 2a, ultrastructural analysis revealed defects in sarcomeric assembly and an embryonic form of dilated cardiomyopathy characterized by a significantly reduced left ventricular ejection fraction in mutant embryos compared with wild type littermates [2].
  • Ventricular tachyarrhythmia could not be induced in either type of mouse [3].
  • Abnormalities in Ca2+ handling, prolonged action potential duration (APD), calcium alternans, and reentrant atrial and ventricular arrhythmias were previously observed with the use of optical mapping of perfused hearts from TNF mice [4].
  • Other changes include atrial enlargement and fibrosis, and diffuse myocytolysis, Physiological analyses using ventricular muscle strip preparations from these mice reveal that both myocardial contraction and relaxation parameters are severely impaired [5].

Psychiatry related information on Myl3

  • These results support the hypothesis that cTnT isoform amino-terminal differences affect myofilament function and suggest that hcTnT(1) expression levels present during human development and in human heart disease can affect in vivo ventricular function [6].
  • They had no or moderate macrocephaly; moderate ventricular dilatation and preserved general motor activity; they all presented spontaneous ventriculostomies communicating the ventricles with the subarachnoid space, indicating that such communications play a key role in the long survival of these mice [7].
  • In a patient whose Creutzfeldt-Jakob disease with congophilic kuru plaques that was proved at necropsy, the early brain CT showed low-density areas in the cerebral white matter before cortical atrophy and ventricular enlargement became apparent [8].
  • However, prior alcohol consumption doubled recovery of left ventricular developed pressure (68 +/- 8 vs. 33 +/- 8 mmHg for controls; n = 10, P < 0.05) and reduced creatine kinase release by half (0.26 +/- 0.04 vs. 0.51 +/- 0.08 U x min(-1) x g wet wt(-1) for controls; n = 10, P < 0.05) [9].

High impact information on Myl3


Chemical compound and disease context of Myl3


Biological context of Myl3

  • Transcripts for the ventricular/slow (MLC1V) and another fast skeletal myosin light chain (MLC3F) are not detected in skeletal muscle before 15 d p.c., which marks the beginning of the fetal stage of muscle development [18].
  • Taken together, this provides evidence for early positional specification of MLC-2v gene expression in the primitive heart tube and indicates regional specification of part of the ventricular muscle gene program can precede ventricular septation during mammalian cardiogenesis [19].
  • To study the process of ventricular specification during cardiogenesis, we examined the in situ expression of cardiac ventricular myosin light chain 2 (MLC-2v) mRNA during murine embryogenesis [19].
  • Morphological analysis of these rescued mice show a moderate pathological phenotype, characterized by atrial myocytolysis; echocardiographic analyses demonstrate altered ventricular functions, such as peak filling rates and left ventricular fractional shortening [20].
  • An increase in left atrial mass, in the absence of transgene expression in that chamber, further supported physiologically abnormal left ventricular diastolic function [1].

Anatomical context of Myl3

  • Like MHC beta, MLC1V transcripts become restricted to ventricular myocytes, but at a slower rate [21].
  • Between 7.5 and 8 d post coitum (p.c.), the newly formed cardiac tube begins to express MHC alpha, MHC beta, MLC1 atrial (MLC1A), and MLC1 ventricular (MLC1V) gene transcripts at high levels throughout the myocardium [21].
  • Sinus node recovery times after carbachol and sinus cycle lengths were shorter and ventricular effective refractory periods were greater in KO mice than in WT mice [3].
  • Decreased fetal cardiac outflow mean velocity, increased proportion of isovolumetric contraction time of the cardiac cycle, and increased pulsatility indices of the descending aorta and inferior vena cava were related to elevated ventricular BNP mRNA levels [22].
  • cTnT1, a cardiac troponin T isoform, decreases myofilament tension and affects the left ventricular pressure waveform [6].

Associations of Myl3 with chemical compounds

  • Recovery kinetics of intracellular Ca(2+) transients recorded from isolated ventricular myocytes at 37 degrees C (tau = 93 +/- 4 ms, n = 18) resembled the APD(90) ERC kinetics [23].
  • The fetal ventricular BNP mRNA levels were about 2.6-fold in the LPS group compared with the control group [22].
  • Our results do not provide evidence to support an extra-cardiac origin of the ventricular CS [24].
  • This resulted in increased basal myocardial adenylyl cyclase activity, enhanced atrial contractility, and increased left ventricular function in vivo; these parameters at baseline in the transgenic animals were equal to those observed in control animals maximally stimulated with isoproterenol [25].
  • Akt-transgenic mice also showed a remarkable increase in cardiac contractility compared with wild-type controls as demonstrated by the analysis of left ventricular (dP/dt(max)) in an invasive hemodynamic study, although with graded dobutamine infusion, the maximum response was not different from that in controls [26].

Physical interactions of Myl3

  • METHODS: Cardiac beta-AR density was measured by [125I]-iodocyanopindolol binding to ventricular membranes [27].
  • The pattern of VSV immunoreactivity supports the idea that following infection of the olfactory bulb glomeruli, VSV spreads via both ventricular surfaces and retrograde transport within axons of neuromodulatory transmitter systems innervating the olfactory bulb [28].

Regulatory relationships of Myl3


Other interactions of Myl3

  • Disparate effects of deficient expression of connexin43 on atrial and ventricular conduction: evidence for chamber-specific molecular determinants of conduction [34].
  • As assessed by hybridization with a specific MLC-2v riboprobe, mRNA expression can be found in the ventricular region at day 8.0 postcoitum (pc) [19].
  • In neonates, MLC2a continues to be expressed around both right and left semilunar valves, the outlet septum and the non-trabeculated right ventricular outlet [30].
  • 3. Results: Stress-induced increases in the PNMT mRNA and protein levels observed in WT mice were almost completely absent in CRH KO mouse adrenal medulla, stellate ganglia, and cardiac atria, while ventricular PNMT mRNA elevation was not CRH-dependent [35].
  • We conclude that Irx4 is not sufficient for ventricular chamber formation but is required for the establishment of some components of a ventricle-specific gene expression program [36].

Analytical, diagnostic and therapeutic context of Myl3

  • Ventricular region-restricted expression of the luciferase reporter in the embryonic heart, as assessed by immunofluorescence and direct assay of reporter activity in microdissected atrial and ventricular muscle specimens, was confirmed from at least day 15 pc on [19].
  • Ventricular ectopy was present only in MyBP-C(t/t) mice during ambulatory ECG recordings [37].
  • In situ hybridization studies during mouse embryogenesis revealed cardiac specific expression throughout days 8-16 postcoitum, with atrial restricted expression from day 12 and qualitatively greater atrial expression than ventricular from day 9 [38].
  • Measurement of the extent and speed of volume displacement of the isotonically contracting hearts with a specially constructed capacitance transducer revealed that ventricular inotropic responsiveness also appeared after 17-19 days [39].
  • In vivo analysis of left ventricular systolic function using M mode and pulsed-wave Doppler echocardiography revealed decreases in fractional shortening (79%) and the normalized mean velocity of circumferential shortening (67%) in transgenic mice compared to wild type (100%) mice [40].


  1. Ventricular expression of a MLC-2v-ras fusion gene induces cardiac hypertrophy and selective diastolic dysfunction in transgenic mice. Hunter, J.J., Tanaka, N., Rockman, H.A., Ross, J., Chien, K.R. J. Biol. Chem. (1995) [Pubmed]
  2. Selective requirement of myosin light chain 2v in embryonic heart function. Chen, J., Kubalak, S.W., Minamisawa, S., Price, R.L., Becker, K.D., Hickey, R., Ross, J., Chien, K.R. J. Biol. Chem. (1998) [Pubmed]
  3. Evaluation of the role of I(KACh) in atrial fibrillation using a mouse knockout model. Kovoor, P., Wickman, K., Maguire, C.T., Pu, W., Gehrmann, J., Berul, C.I., Clapham, D.E. J. Am. Coll. Cardiol. (2001) [Pubmed]
  4. Electrical remodeling of cardiac myocytes from mice with heart failure due to the overexpression of tumor necrosis factor-alpha. Petkova-Kirova, P.S., Gursoy, E., Mehdi, H., McTiernan, C.F., London, B., Salama, G. Am. J. Physiol. Heart Circ. Physiol. (2006) [Pubmed]
  5. Beta-tropomyosin overexpression induces severe cardiac abnormalities. Muthuchamy, M., Boivin, G.P., Grupp, I.L., Wieczorek, D.F. J. Mol. Cell. Cardiol. (1998) [Pubmed]
  6. cTnT1, a cardiac troponin T isoform, decreases myofilament tension and affects the left ventricular pressure waveform. Nassar, R., Malouf, N.N., Mao, L., Rockman, H.A., Oakeley, A.E., Frye, J.R., Herlong, J.R., Sanders, S.P., Anderson, P.A. Am. J. Physiol. Heart Circ. Physiol. (2005) [Pubmed]
  7. Heterogeneous expression of hydrocephalic phenotype in the hyh mice carrying a point mutation in alpha-SNAP. Bátiz, L.F., Páez, P., Jiménez, A.J., Rodríguez, S., Wagner, C., Pérez-Fígares, J.M., Rodríguez, E.M. Neurobiol. Dis. (2006) [Pubmed]
  8. Creutzfeldt-Jakob disease with congophilic kuru plaques: CT and pathological findings of the cerebral white matter. Kawata, A., Suga, M., Oda, M., Hayashi, H., Tanabe, H. J. Neurol. Neurosurg. Psychiatr. (1992) [Pubmed]
  9. Moderate alcohol consumption induces sustained cardiac protection by activating PKC-epsilon and Akt. Zhou, H.Z., Karliner, J.S., Gray, M.O. Am. J. Physiol. Heart Circ. Physiol. (2002) [Pubmed]
  10. The homeodomain transcription factor Irx5 establishes the mouse cardiac ventricular repolarization gradient. Costantini, D.L., Arruda, E.P., Agarwal, P., Kim, K.H., Zhu, Y., Zhu, W., Lebel, M., Cheng, C.W., Park, C.Y., Pierce, S.A., Guerchicoff, A., Pollevick, G.D., Chan, T.Y., Kabir, M.G., Cheng, S.H., Husain, M., Antzelevitch, C., Srivastava, D., Gross, G.J., Hui, C.C., Backx, P.H., Bruneau, B.G. Cell (2005) [Pubmed]
  11. Nkx2-5 pathways and congenital heart disease; loss of ventricular myocyte lineage specification leads to progressive cardiomyopathy and complete heart block. Pashmforoush, M., Lu, J.T., Chen, H., Amand, T.S., Kondo, R., Pradervand, S., Evans, S.M., Clark, B., Feramisco, J.R., Giles, W., Ho, S.Y., Benson, D.W., Silberbach, M., Shou, W., Chien, K.R. Cell (2004) [Pubmed]
  12. FKBP12.6 deficiency and defective calcium release channel (ryanodine receptor) function linked to exercise-induced sudden cardiac death. Wehrens, X.H., Lehnart, S.E., Huang, F., Vest, J.A., Reiken, S.R., Mohler, P.J., Sun, J., Guatimosim, S., Song, L.S., Rosemblit, N., D'Armiento, J.M., Napolitano, C., Memmi, M., Priori, S.G., Lederer, W.J., Marks, A.R. Cell (2003) [Pubmed]
  13. Molecular insights from a novel cardiac troponin I mouse model of familial hypertrophic cardiomyopathy. Tsoutsman, T., Chung, J., Doolan, A., Nguyen, L., Williams, I.A., Tu, E., Lam, L., Bailey, C.G., Rasko, J.E., Allen, D.G., Semsarian, C. J. Mol. Cell. Cardiol. (2006) [Pubmed]
  14. Overexpression of angiotensin II type I receptor in cardiomyocytes induces cardiac hypertrophy and remodeling. Paradis, P., Dali-Youcef, N., Paradis, F.W., Thibault, G., Nemer, M. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  15. In vivo cardiac electrophysiology studies in the mouse. Berul, C.I., Aronovitz, M.J., Wang, P.J., Mendelsohn, M.E. Circulation (1996) [Pubmed]
  16. Pressure overload induces severe hypertrophy in mice treated with cyclosporine, an inhibitor of calcineurin. Ding, B., Price, R.L., Borg, T.K., Weinberg, E.O., Halloran, P.F., Lorell, B.H. Circ. Res. (1999) [Pubmed]
  17. The antioxidant N-2-mercaptopropionyl glycine attenuates left ventricular hypertrophy in in vivo murine pressure-overload model. Date, M.O., Morita, T., Yamashita, N., Nishida, K., Yamaguchi, O., Higuchi, Y., Hirotani, S., Matsumura, Y., Hori, M., Tada, M., Otsu, K. J. Am. Coll. Cardiol. (2002) [Pubmed]
  18. 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]
  19. 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]
  20. Rescue of high expression beta-tropomyosin transgenic mice by 5-propyl-2-thiouracil. Regulating the alpha-myosin heavy chain promoter. Prabhakar, R., Boivin, G.P., Hoit, B., Wieczorek, D.F. J. Biol. Chem. (1999) [Pubmed]
  21. Developmental regulation of myosin gene expression in mouse cardiac muscle. Lyons, G.E., Schiaffino, S., Sassoon, D., Barton, P., Buckingham, M. J. Cell Biol. (1990) [Pubmed]
  22. Fetal cardiac natriuretic peptide expression and cardiovascular hemodynamics in endotoxin-induced acute cardiac dysfunction in mouse. Mäkikallio, K., Rounioja, S., Vuolteenaho, O., Paakkari, J., Hallman, M., Räsänen, J. Pediatr. Res. (2006) [Pubmed]
  23. Action potential characterization in intact mouse heart: steady-state cycle length dependence and electrical restitution. Knollmann, B.C., Schober, T., Petersen, A.O., Sirenko, S.G., Franz, M.R. Am. J. Physiol. Heart Circ. Physiol. (2007) [Pubmed]
  24. Molecular characterization of the ventricular conduction system in the developing mouse heart: topographical correlation in normal and congenitally malformed hearts. Franco, D., Icardo, J.M. Cardiovasc. Res. (2001) [Pubmed]
  25. Enhanced myocardial function in transgenic mice overexpressing the beta 2-adrenergic receptor. Milano, C.A., Allen, L.F., Rockman, H.A., Dolber, P.C., McMinn, T.R., Chien, K.R., Johnson, T.D., Bond, R.A., Lefkowitz, R.J. Science (1994) [Pubmed]
  26. Akt induces enhanced myocardial contractility and cell size in vivo in transgenic mice. Condorelli, G., Drusco, A., Stassi, G., Bellacosa, A., Roncarati, R., Iaccarino, G., Russo, M.A., Gu, Y., Dalton, N., Chung, C., Latronico, M.V., Napoli, C., Sadoshima, J., Croce, C.M., Ross, J. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  27. L-type calcium current and contractility in ventricular myocytes from mice overexpressing the cardiac beta 2-adrenoceptor. Heubach, J.F., Trebess, I., Wettwer, E., Himmel, H.M., Michel, M.C., Kaumann, A.J., Koch, W.J., Harding, S.E., Ravens, U. Cardiovasc. Res. (1999) [Pubmed]
  28. Distribution of vesicular stomatitis virus proteins in the brains of BALB/c mice following intranasal inoculation: an immunohistochemical analysis. Huneycutt, B.S., Plakhov, I.V., Shusterman, Z., Bartido, S.M., Huang, A., Reiss, C.S., Aoki, C. Brain Res. (1994) [Pubmed]
  29. Expression patterns of Brx1 (Rieg gene), Sonic hedgehog, Nkx2.2, Dlx1 and Arx during zona limitans intrathalamica and embryonic ventral lateral geniculate nuclear formation. Kitamura, K., Miura, H., Yanazawa, M., Miyashita, T., Kato, K. Mech. Dev. (1997) [Pubmed]
  30. Myosin light chain 2a and 2v identifies the embryonic outflow tract myocardium in the developing rodent heart. Franco, D., Markman, M.M., Wagenaar, G.T., Ya, J., Lamers, W.H., Moorman, A.F. Anat. Rec. (1999) [Pubmed]
  31. Downregulation of atrial markers during cardiac chamber morphogenesis is irreversible in murine embryos. Gruber, P.J., Kubalak, S.W., Chien, K.R. Development (1998) [Pubmed]
  32. Patterning the embryonic heart: identification of five mouse Iroquois homeobox genes in the developing heart. Christoffels, V.M., Keijser, A.G., Houweling, A.C., Clout, D.E., Moorman, A.F. Dev. Biol. (2000) [Pubmed]
  33. Versican expression is associated with chamber specification, septation, and valvulogenesis in the developing mouse heart. Henderson, D.J., Copp, A.J. Circ. Res. (1998) [Pubmed]
  34. Disparate effects of deficient expression of connexin43 on atrial and ventricular conduction: evidence for chamber-specific molecular determinants of conduction. Thomas, S.A., Schuessler, R.B., Berul, C.I., Beardslee, M.A., Beyer, E.C., Mendelsohn, M.E., Saffitz, J.E. Circulation (1998) [Pubmed]
  35. 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]
  36. Cardiomyopathy in Irx4-deficient mice is preceded by abnormal ventricular gene expression. Bruneau, B.G., Bao, Z.Z., Fatkin, D., Xavier-Neto, J., Georgakopoulos, D., Maguire, C.T., Berul, C.I., Kass, D.A., Kuroski-de Bold, M.L., de Bold, A.J., Conner, D.A., Rosenthal, N., Cepko, C.L., Seidman, C.E., Seidman, J.G. Mol. Cell. Biol. (2001) [Pubmed]
  37. Ventricular arrhythmia vulnerability in cardiomyopathic mice with homozygous mutant Myosin-binding protein C gene. Berul, C.I., McConnell, B.K., Wakimoto, H., Moskowitz, I.P., Maguire, C.T., Semsarian, C., Vargas, M.M., Gehrmann, J., Seidman, C.E., Seidman, J.G. Circulation (2001) [Pubmed]
  38. Chamber specification of atrial myosin light chain-2 expression precedes septation during murine cardiogenesis. Kubalak, S.W., Miller-Hance, W.C., O'Brien, T.X., Dyson, E., Chien, K.R. J. Biol. Chem. (1994) [Pubmed]
  39. Responsiveness to glucagon in fetal hearts. Species variability and apparent disparities between changes in beating, adenylate cyclase activation, and cyclic AMP concentration. Wildenthal, K., Allen, D.O., Karlsson, J., Wakeland, J.R., Clark, C.M. J. Clin. Invest. (1976) [Pubmed]
  40. Cardiac-specific overexpression of phospholamban alters calcium kinetics and resultant cardiomyocyte mechanics in transgenic mice. Kadambi, V.J., Ponniah, S., Harrer, J.M., Hoit, B.D., Dorn, G.W., Walsh, R.A., Kranias, E.G. J. Clin. Invest. (1996) [Pubmed]
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