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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Cmya5tm1Cap
targeted mutation 1, Yassemi Capetanaki
MGI:7261228
Summary 1 genotype
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Cmya5tm1Cap/Cmya5tm1Cap 129-Cmya5tm1Cap MGI:7261290


Genotype
MGI:7261290
hm1
Allelic
Composition
Cmya5tm1Cap/Cmya5tm1Cap
Genetic
Background
129-Cmya5tm1Cap
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cmya5tm1Cap mutation (0 available); any Cmya5 mutation (148 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• 6- to 12-month-old mice, to a larger extent in older mice
• severe mitochondrial structural defects including inter-mitochondrial vacuoles, cristae disorganization and blebbing, and extensive cristolysis that are more pronounced in the left ventricle
• some abnormal nuclei shape and positioning (unusually attached to the mitochondrial
• however, sarcomeres are well-aligned and organized
• discontinuous, fragmented, and disorganized
• 9- to 12-month-old mice
• 6- to 12-month-old mice, to a larger extent in older mice
• female mice are more affected than male mice

behavior/neurological
N
• male mice exhibit normal recognition and spatial memory and performance in an elevated plus maze
• decreased sucrose preference in male mice
• in male mice with decreased exploration in an open field
• in male mice
• lack of preference for the conspecific in male mice
• however, social novelty preference is normal

nervous system
• 3-month-old mice exhibit less compact neuropil with ultrastructural abnormalities, fewer presynaptic vesicles, fewer neurofilaments, and fragmented mitochondrial at synaptic junctions, and abnormal accumulation of membranous interconnected tubules compared with wild-type mice
• swollen with fragmented and degenerating mitochondrial and disorganized neurofilaments in the molecular layer of 3-month-old mice
• subtle in male mice

homeostasis/metabolism
• decreased dopamine turnover in the striatum
• increased dopamine turnover in the prefrontal cortex
• in the striatum and prefrontal cortex

muscle
• severe mitochondrial structural defects including inter-mitochondrial vacuoles, cristae disorganization and blebbing, and extensive cristolysis that are more pronounced in the left ventricle
• some abnormal nuclei shape and positioning (unusually attached to the mitochondrial
• however, sarcomeres are well-aligned and organized
• discontinuous, fragmented, and disorganized
• female mice are more affected than male mice
• severe mitochondrial defects
• severe mitochondrial defects, especially in the soleus
• dilated with loss of SR-mitochondrial contact sites

pigmentation
• in the cerebellum of 3-month-old mice

limbs/digits/tail
• severe mitochondrial defects
• severe mitochondrial defects, especially in the soleus

cellular
• 6- to 12-month-old mice, to a larger extent in older mice





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last database update
05/07/2024
MGI 6.23
The Jackson Laboratory