About   Help   FAQ
Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Myh10tm3Rsad
targeted mutation 3, Robert S Adelstein
MGI:3052104
Summary 1 genotype
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Myh10tm3Rsad/Myh10tm3Rsad involves: 129S6/SvEvTac * C57BL/6 MGI:3052311


Genotype
MGI:3052311
hm1
Allelic
Composition
Myh10tm3Rsad/Myh10tm3Rsad
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Myh10tm3Rsad mutation (0 available); any Myh10 mutation (95 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• most mutant pups die within two days of birth with less than 10% surviving to P15 (only 1 survived to P20)

behavior/neurological
• ataxia manifests as a wide gait and impaired balance
• mutants are unable to balance on a rotorod

cardiovascular system
• at E12.5 the percentage of binucleated cells is increased to 23% from 1% in wild-type and the size of the myocytes is increased

nervous system
• granule cells migration out of the EGL is slower in mutants compared to wild-type
• pontine neurons fail to reach the basilar pons at P0 and are instead found to accumulate along with reticular neurons under the pial surfarce in the lateral posterior area of the medulla
• abnormal accumulation of neurons from the posterior extramural migratory stream is also seen
• progressive hydroencephaly is seen by P3 (J:92081)
• mice show severe hydroencephaly (J:112536)
• mice show protrusion of facial neurons into fourth ventricle
• at P12 a distorted cerebral cortex is seen
• at P0 fissures are shallower than normal and those at folia II, III, VII, and VIII are absent
• at P8 fissures in the anterior and middle portion are shallower or absent while those in the posterior portion look almost normal
• at P0 the EGL is thinner than normal however by P8 the thickness is comparable and by P15 the EGL is more prominent compared to wild-type
• cerebellar Purkinje cells are smaller and irregularly aligned
• at P8 the mutant IGL is about half the thickness of wild-type
• a reduced number of migrating granule cells are seen at P8
• at P12 a small cerebellum is seen
• at P0 the facial neurons are diminished with most failing to reach their normal location and instead forming a mass the protrudes into the fourth ventricle

cellular
• granule cells migration out of the EGL is slower in mutants compared to wild-type
• pontine neurons fail to reach the basilar pons at P0 and are instead found to accumulate along with reticular neurons under the pial surfarce in the lateral posterior area of the medulla
• abnormal accumulation of neurons from the posterior extramural migratory stream is also seen

growth/size/body
N
• embryos DO NOT exhibit defects in ventral body wall closure or midline fusion





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
Citing These Resources
Funding Information
Warranty Disclaimer, Privacy Notice, Licensing, & Copyright
Send questions and comments to User Support.
last database update
11/12/2024
MGI 6.24
The Jackson Laboratory