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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Vegfatm2Pec
targeted mutation 2, Peter Carmeliet
MGI:2136623
Summary 2 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Vegfatm2Pec/Vegfatm2Pec involves: 129S1/Sv * 129X1/SvJ MGI:3796444
cx2
Tg(SOD1*G93A)1Gur/0
Vegfatm2Pec/Vegfatm2Pec
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:4831157


Genotype
MGI:3796444
hm1
Allelic
Composition
Vegfatm2Pec/Vegfatm2Pec
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Vegfatm2Pec mutation (0 available); any Vegfa mutation (20 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 60% die before or around birth while the remaining 40% survive more than 23 months
• 60% die before or around birth while the remaining 40% survive more than 23 months

growth/size/body
• surviving mutants are about 25% smaller at birth
• surviving mutants gain about 45% less weight than wild-type

behavior/neurological
• mutants develop coarse fur indicative of impaired grooming
• mutants have difficulty turning over when placed on their backs at 5 months of age and can hardly turn over at all by 15 months of age
• when lifted by the tail, mutants reflexively contract their limbs to the trunk and remain immobile
• in the grid test, mutants fall off the grid much quicker than wild-type
• mutants perform worse in the rotating axle test, falling off much quicker than wild-type
• mutants have difficulties in grabbing a horizontal thread with their hindlimbs and hang immobile, while wild-type immediately grab the thread
• mutants are less active at night and for much shorter periods than wild-type
• mutants slap their paws while walking and have a waddling gait
• severely paralysis after ischemic insult by clamping the aortic arch, left subclavian artery and internal mammary artery for only 8 min
• no recovery neurologically
• mutants show progressive signs of limb paresis
• older males are sexually inactive, possibly due to motor dysfunction

muscle
• progressive skeletal muscle fiber atrophy after 4 months of age; atrophy is specific for extrafusal muscle fibers and does not affect muscle spindles or cardiac muscle fibers
• however show no signs of fiber necrosis, sarcomere lysis or sarcolemma disruption, fatty infiltration, fibrosis or dystrophic calcification
• the ankle dorsal flexor muscles of old mice generate only 65% of the maximal force upon tetanic stimulation
• latencies of compound muscle action potentials are slightly increased
• mutants become progressively less mobile and show signs of severe muscle weakness and limb paresis
• muscle weakness is not due to impaired oxygenation or reduced levels of hemoglobin

nervous system
• prominent reactive astrocytosis in the ventral horn of the spinal cord is seen beyond 7 months of age
• focal spheroid axon swellings often occur in several cranial motor nerves and in the ventral horns of the spinal cords beyond 7 months of age
• mutants show features of Wallerian degeneration, including shrunken vacuolated axoplasm, disorganized neurofilaments, few abnormal mitochondria, endoneural fibrosis, and infiltration of macrophages
• aberrant neurofilament accumulation is seen in the motor, but not sensory, nuclei or roots of several cranial nerves in mutants older than 7 months of age
• phrenic nerves progressively lose their large myelinated Agamma motor axons, which innervate the extrafusal muscle fibers
• sciatic nerves progressively lose their large myelinated Agamma motor axons, which innervate the extrafusal muscle fibers
• phosphorylated neurofilament inclusions are seen in the ventral horns of older mutants
• neurodegeneration is due to reduced neural vascular perfusion
• surviving mutants appear healthy until 5 months of age, when they develop progressive motor neuron degeneration of lower motor neurons
• motor neuron degeneration occurs especially in the ventral horn of the spinal cord (30% loss at 17 months) and the motor nuclei in the brain stem
• loss of motor axons in peripheral nerves
• sciatic and phrenic nerves progressively lose their large myelinated Agamma motor axons, which innervate the extrafusal muscle fiber

reproductive system

skeleton

cardiovascular system
• in skeletal muscle, capillary lumen sizes are smaller
• however, capillary-to-muscle ratios, fluoroangiography, and microvascular partial oxygen pressure were normal, indicating that motor neuron degeneration is not secondary to muscle ischemia
• laser Doppler measurements show that baseline neural blood flow is lower than in wild-type, even though the neural vascular flow similarly increases by about 40% in response to hypercapnia, indicating a deficit in neural vascular perfusion

integument
• mutants develop coarse fur indicative of impaired grooming

respiratory system
• a small fraction of mutants that die at birth exhibit lung prematurity
• in a small fraction of mutants, a significantly increased alveolar septal thickness is noted at birth
• in a small fraction of mutants, lung aeration (percentage of total surface filled with air) fails to increase after birth

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
amyotrophic lateral sclerosis type 1 DOID:0060193 OMIM:105400
J:69797




Genotype
MGI:4831157
cx2
Allelic
Composition
Tg(SOD1*G93A)1Gur/0
Vegfatm2Pec/Vegfatm2Pec
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(SOD1*G93A)1Gur mutation (3 available)
Vegfatm2Pec mutation (0 available); any Vegfa mutation (20 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• die earlier (107 3 d) than Tg(SOD1*G93A)1Gur mice

muscle
• worse muscle weakness than Tg(SOD1*G93A)1Gur mice

behavior/neurological
• perform worse in the rotarod test (unable to stay for 2 min on the rotarod beyond 98 2 d) than Tg(SOD1*G93A)1Gur mice





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last database update
10/17/2017
MGI 6.10
The Jackson Laboratory