Phenotypes associated with this allele

• Allele Symbol: Lzts1^tm1Kso
• Allele Name: targeted mutation 1, Kenji Sobue
• Allele ID: MGI:5700365
• Summary: 1 genotype

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Lzts1^tm1Kso/Lzts1^tm1Kso	B6J.B6NTac-Lzts1^tm1Kso	MGI:5706982

Genotype
MGI:5706982

hm1

• Allelic Composition: Lzts1^tm1Kso/Lzts1^tm1Kso
• Genetic Background: B6J.B6NTac-Lzts1^tm1Kso

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

behavior/neurological

behavior/neurological phenotype ( J:226686 )

N • homozygotes show no significant alterations in sociability in the three-chamber social interaction test

abnormal object recognition memory ( J:226686 )

• in a novel object recognition test, homozygotes show a lower preference to access a novel object

abnormal spatial working memory ( J:226686 )

• in the Y-maze test, homozygotes show normal locomotor activity, but their alternation score is significantly reduced relative to wild-type controls

increased anxiety-related response ( J:226686 )

• in the open-field test, homozygotes exhibit normal spontaneous locomotor activity but show a significant tendency to avoid entry into the center zone relative to wild-type controls

• in an elevated plus maze test, homozygotes show a significant tendency to avoid entering open arms, with shorter durations and track lengths in the open arms

nervous system

abnormal CNS synapse formation ( J:226686 )

• homozygotes display defects in nascent spine synapse maturation and increases in nonfunctional immature synapses

abnormal dendritic spine morphology ( J:226686 )

• Golgi staining for pyramidal neurons in layer 2/3 of the medial prefrontal cortex (mPFC) showed that the frequency of thin-headed spines in both the apical and basal dendrites as well as spine density are significantly increased

• in primary cultured neurons from the frontal cortex, the frequency of thin spines is increased whereas that of mushroom-type spines is decreased relative to wild-type neurons

abnormal CNS synaptic transmission ( J:226686 )

• at 8-12 weeks of age, homozygotes display defects in AMPAR-mediated glutamatergic synaptic transmission

• impaired glutamatergic synapse transmission is accompanied by tiny-headed immature dendritic spines, due to aberrant Rap2 activation in the prefrontal cortex

• Rap2 inactivation in the mPFC ameliorates the behavioral defects in spatial working memory and enhanced anxiety but has little effect on the cognition defect assessed by the novel object recognition test

prolonged excitatory postsynaptic current decay time ( J:226686 )

• decays of EPSCs at +40 mV are prolonged in mutant pyramidal neurons on layer 2/3 of the mPFC

abnormal glutamate-mediated receptor currents ( J:226686 )

• the AMPAR/NMDAR ratio, calculated as the ratio of the amplitude of EPSCs at -70 mV to that of EPSCs at +40 mV, is reduced in mutant synapses on layer 2/3 pyramidal cells of the mPFC

abnormal miniature excitatory postsynaptic currents ( J:226686 )

• at 8-12 weeks of age, electrophysiological recordings from mutant pyramidal cells in layer 2/3 of the mPFC revealed that, although the mean mEPSC amplitude is normal, the mEPSC frequency is reduced by >50%

neoplasm

increased tumor incidence ( J:226686 )

• although homozygotes are viable, fertile and able to reach maturity, they develop various tumors at approximately 18 months of age

• data presented in J:226686 were obtained before the onset of tumors