Ventricular myosin light chain 2, encoded by the Myl2 gene, is essential in vertebrate smooth muscle contraction and has a regulatory role in striated slow twitch muscle contraction. Mutations in this gene have been associated with hypertrophic cardiomyopathy.
This strain expresses Cre recombinase from the endogenous Myl2 locus. Cre recombinase activity is detected in cardiac ventricular muscle starting at day E8.75. Myl2 expression initiates at E7.5 in the ventricular cardiac primordia. Heterozygous knock-in/knock-out mice are viable and fertile. Mice that are homozygous for the knock-in mutation have an embryonic lethal phenotype, dying at approximately E12.5.
The Mlc2v-cre knock-in/knock-out allele has a Cre recombinase gene which replaced part of exon 1 and all of exon 2 of the Myl2 gene; both abolishing endogenous Myl2 gene function and placing cre expression under the control of the endogenous Myl2 promoter/enhancer elements. Cre recombinase expression is directed at the cardiac ventricular muscle starting at approximately E8.
These mice may be useful for Cre-lox studies of cardiogenesis.
The mice are designated Tangible Research Material (TRM). A complete description, including genotyping, phenotyping, etc is found at The Jackson Lab cat. No. 029465 https://www.jax.org/strain/029465
Academic and non-profit institutions please order directly from The Jackson Laboratory. Commercial entities require a license from UC San Diego contact ( https://innovation.ucsd.edu/contact/).
Hypertrophic cardiomyopathy, smooth muscle, muscle contraction, Myl2 gene, myosin light chain 2, murine cardiogenesis