Phenotypes Associated with This Genotype

Genotype
MGI:3524779

• Allelic Composition: Serpine2^tm1Dmn/Serpine2^tm1Dmn
• Genetic Background: B6.129P2-Serpine2^tm1Dmn

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

behavior/neurological

abnormal motor capabilities/coordination/movement ( J:94811 )

• normal level of activity, balance, speed and coordination

abnormal sensory capabilities/reflexes/nociception ( J:94811 )

• mutants need significantly more time to perform a whisker-sensitive task than wild-type

• whisker trimming did not impair the distance crossed in gap-crossing test as it did in wild-type

nervous system

abnormal cerebellum external granule cell layer morphology ( J:121263 )

• while the overall thickness of the external granular layer (EGL) is unchanged, the outer EGL is thickened and the inner EGL is thinned noticeably at P5 and obviously by P10

• cerebellar granular neuron precursor (CGNP) differentiation is delayed

• proliferating CGNPs are restricted to the pial surface whereas in wild-type mice they are evenly spread through out the outer EGL

abnormal cerebellar granule layer morphology ( J:121263 )

• at P10, the thickness of the inner granular layer (IGL) is increased in the anterior-central part of the cerebellum by 67%

• at P10, the medial cerebellum is most affected by volume increase

• in adult mice, the width of the IGL in posterior lobe VIII is increased by 40% and the IGL of lobe VI is 60% thicker

• mice have a 6% increase in IGL volume at P10 and by adulthood the increase reached 12.2%

• volume increase in the anterior, medial and posterior lobes of the cerebellum are 11.3%, 9.3% and 15.4%, respectively, in adults lobe IX protrudes more than in wild-type mice

abnormal astrocyte morphology ( J:121263 )

• Bergmann glial cell fibers have increased thickness, appear irregular and contact the pial surface with larger endfeet in comparison to wild-type

decreased Schwann cell number ( J:121223 )

• following crush damage, Schwann cell proliferation is decreased and apoptosis rates are increased

abnormal sciatic nerve morphology ( J:121223 )

• at 12 days following sciatic nerve crush, axonal regeneration in the sciatic nerve in the triceps surae muscle is delayed

• responsiveness following injury is delayed and mice do not regain full use of their limb until 2 to 4 days later than wild-type mice

delayed peripheral nervous system regeneration ( J:121223 )

• at 12 days following sciatic nerve crush, axonal regeneration in the sciatic nerve in the triceps surae muscle is delayed

• responsiveness following injury is delayed and mice do not regain full use of their limb until 2 to 4 days later than wild-type mice

reduced NMDA receptor mediated synaptic activity in barrel cortex ( J:94811 )

• decreased sensory-evoked potential in the somatosensory cortex

abnormal excitatory postsynaptic currents ( J:94811 )

• strong reduction in excitatory postsynaptic currents at +40 mV compared to wild-type but no difference from wild-type at 60 mV, indicating a deficiency in NMDA receptors

cellular

increased cell proliferation ( J:121263 )

• in vitro, cerebrellar granular neuron precursors (CGNPs) and glial cells a two-fold higher basal proliferative rate and a much stronger proliferative response compared to wild-type cells following Shh treatment

• in vitro, CGNPs show a 28% increase in proliferation

homeostasis/metabolism

abnormal acute phase protein level ( J:121263 )

• fibrin accumulates following peripheral nerve damage

abnormal response to injury ( J:121223 )

• at 12 days following sciatic nerve crush, axonal regeneration in the sciatic nerve in the triceps surae muscle is delayed

• responsiveness following injury is delayed and mice do not regain full use of their limb until 2 to 4 days later than wild-type mice

• following crush damage, Schwann cell proliferation is decreased and apoptosis rates are increased

immune system

abnormal acute phase protein level ( J:121263 )

• fibrin accumulates following peripheral nerve damage