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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Myh11tm1Bdr
targeted mutation 1, Michael Bader
MGI:2656492
Summary 1 genotype
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Myh11tm1Bdr/Myh11tm1Bdr Not Specified MGI:2656497


Genotype
MGI:2656497
hm1
Allelic
Composition
Myh11tm1Bdr/Myh11tm1Bdr
Genetic
Background
Not Specified
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Myh11tm1Bdr mutation (0 available); any Myh11 mutation (93 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• most homozygotes die within 12-24 hrs of birth, possibly due to renal failure
• however, homozygotes can survive for up to 72 hrs (without growing normally) when their bladders are emptied by external pressure

growth/size/body
• although neonates (4-6 hrs) are of normal size and weight, P3 homozygotes fail to gain weight to the same extent as wild-type littermates

renal/urinary system
• prolonged activation by KCl depolarisation of intact bladder preparations from homozygous mutant neonates indicates absence of the initial transient state of of high force generation and maximal shortening velocity (phase 1)
• in contrast, phase 2, a subsequent sustained state characterized by low force generation and maximal shortening velocity remains normal, suggesting that in neonatal smooth muscle phase 1 is generated by recruitment of smooth-muscle myosin heavy chain (MHC), whereas phase 2 can be generated by activation of non-muscle MHC
• at ~9 hrs after birth, homozygotes show a filled, giant, thin-walled bladder
• at ~9 hrs after birth
• newborn homozygotes are unable to urinate

muscle
• newborn homozygotes exhibit a dilative cardiomyopathy, putatively due to a 3-hr delay in ductus arteriosus closure
• milk obtained from mothers remains in the stomach and upper duodenum, probably as a result of reduced intestinal movement
• low intestinal motility is probably responsible for starvation in growth-impaired neonates
• prolonged activation by KCl depolarisation of intact bladder preparations from homozygous mutant neonates indicates absence of the initial transient state of of high force generation and maximal shortening velocity (phase 1)
• in contrast, phase 2, a subsequent sustained state characterized by low force generation and maximal shortening velocity remains normal, suggesting that in neonatal smooth muscle phase 1 is generated by recruitment of smooth-muscle myosin heavy chain (MHC), whereas phase 2 can be generated by activation of non-muscle MHC

cardiovascular system
• newborn homozygotes display a 3-hr delay in ductus arteriosus closure relative to wild-type littemates
• newborn homozygotes display a giant left ventricular cavity
• newborn homozygotes exhibit a thin free left ventricular wall relative to wild-type mice
• newborn homozygotes exhibit a dilative cardiomyopathy, putatively due to a 3-hr delay in ductus arteriosus closure
• elevated plasma renin levels indicate that mean arterial blood pressure may be severely reduced

homeostasis/metabolism
• newborn homozygotes exhibit a ~4-fold increase in plasma renin levels relative to wild-type mice

digestive/alimentary system
• milk obtained from mothers remains in the stomach and upper duodenum, probably as a result of reduced intestinal movement
• low intestinal motility is probably responsible for starvation in growth-impaired neonates

integument
• newborn homozygotes appear pale

cellular
• newborn homozygotes display a 3-hr delay in ductus arteriosus closure relative to wild-type littemates





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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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last database update
04/23/2024
MGI 6.23
The Jackson Laboratory