All Phenotypes Cfl1<tm1.1Wit> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Cfl1^tm1.1Wit/Cfl1^tm1.1Wit	involves: 129 * C57BL/6 * SJL	MGI:4943295
cn2	Cfl1^tm1.1Wit/Cfl1⁺ Dstn^tm1.1Wit/Dstn^tm1.1Wit Tg(Nes-cre)1Kln/0	involves: 129 * BALB/cJ * C57BL/6 * SJL	MGI:4943294
cn3	Cfl1^tm1.1Wit/Cfl1^tm1.1Wit Tg(NPHS2-cre)295Lbh/0	involves: 129 * C57BL/6 * SJL	MGI:5432555
cn4	Cap1^tm1.1Mbrst/Cap1^tm1.1Mbrst Cfl1^tm1.1Wit/Cfl1^tm1.1Wit Tg(Nes-cre)1Kln/0	involves: 129 * C57BL/6 * SJL	MGI:7443115

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

mortality/aging

premature death ( J:125317 )

• rare survivors die by P30

postnatal lethality, incomplete penetrance ( J:125317 )

• nearly all mice die by between P1 and P3

nervous system

seizures ( J:125317 )

• in rare survivors

abnormal neuron differentiation ( J:125317 )

• neuronal progenitors exit the cell cycle prematurely and differentiate

abnormal axon extension ( J:125317 )

• neurite outgrowth is impaired compared to in wild-type mice

premature neuronal precursor differentiation ( J:125317 )

• between E13 and E19, neuronal progenitor cells in the ventricular zone exhibit a migratory defect that prevents them from entering intermediate layers unlike in wild-type mice

• at E18, radial migration of proliferating cells into the cortex is impaired compared to in wild-type mice

• neuronal progenitors fail to reach the medial pallium unlike in wild-type mice

• interkinetic nuclear migration in the ventricular zone is impaired compared to in wild-type mice

abnormal neuronal precursor proliferation ( J:125317 )

• at E14 and E16, mice exhibit impaired cell proliferation of cells in the ventricular zone compared to in wild-type mice

enlarged brain ventricles ( J:125317 )

abnormal cerebral cortex morphology ( J:125317 )

• large parts of layers II, III, and IV are missing compared with wild-type mice

• however, the upper molecular layer I and the inner multiform layer VI are present

abnormal neurite morphology ( J:125317 )

• neurites are shorter than in wild-type cells

behavior/neurological

ataxia ( J:125317 )

• in rare survivors

seizures ( J:125317 )

• in rare survivors

growth/size/body

postnatal growth retardation ( J:125317 )

• in rare survivors

cellular

abnormal neuron differentiation ( J:125317 )

• neuronal progenitors exit the cell cycle prematurely and differentiate

abnormal axon extension ( J:125317 )

• neurite outgrowth is impaired compared to in wild-type mice

premature neuronal precursor differentiation ( J:125317 )

• between E13 and E19, neuronal progenitor cells in the ventricular zone exhibit a migratory defect that prevents them from entering intermediate layers unlike in wild-type mice

• at E18, radial migration of proliferating cells into the cortex is impaired compared to in wild-type mice

• neuronal progenitors fail to reach the medial pallium unlike in wild-type mice

• interkinetic nuclear migration in the ventricular zone is impaired compared to in wild-type mice

abnormal neuronal precursor proliferation ( J:125317 )

• at E14 and E16, mice exhibit impaired cell proliferation of cells in the ventricular zone compared to in wild-type mice

Allelic Composition	Cfl1^tm1.1Wit/Cfl1⁺ Dstn^tm1.1Wit/Dstn^tm1.1Wit Tg(Nes-cre)1Kln/0
Genetic Background	involves: 129 * BALB/cJ * C57BL/6 * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cfl1^tm1.1Wit mutation (0 available); any Cfl1 mutation (25 available)
Dstn^tm1.1Wit mutation (0 available); any Dstn mutation (43 available)
Tg(Nes-cre)1Kln mutation (4 available)

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

normal phenotype

no abnormal phenotype detected ( J:125317 )

• mice are viable and phenotypically normal

Allelic Composition	Cfl1^tm1.1Wit/Cfl1^tm1.1Wit Tg(NPHS2-cre)295Lbh/0
Genetic Background	involves: 129 * C57BL/6 * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cfl1^tm1.1Wit mutation (0 available); any Cfl1 mutation (25 available)
Tg(NPHS2-cre)295Lbh mutation (3 available)

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

mortality/aging

premature death ( J:165315 )

• mice exhibit a reduced life span with a median age at death of 9 months

homeostasis/metabolism

increased circulating creatinine level ( J:165315 )

• significant increase in serum creatinine levels at 6 months of age, indicating renal dysfunction

ascites ( J:165315 )

• large ascites detected at 9 months of age

increased urine protein level ( J:165315 )

• mice develop persistent proteinuria by 3 months of age

• rate of proteinuria increases modestly until 6 months and accelerates more rapidly thereafter

abnormal response to injury ( J:165315 )

• after induction of kidney podocyte injury by protamine sulfate (PS) perfusion, mutant foot processes exhibit a broadened and flattened morphology that is distinct from that in wild-type controls

• PS-treated mutant podocytes develop unusually long fine processes that project from primary, secondary, and tertiary processes, suggesting pseudovillous transformation

• PS-treated mutant podocytes fail to recover normal morphology following subsequent infusion of heparin sulfate, unlike wild-type controls

renal/urinary system

renal/urinary system phenotype ( J:165315 )

N	• mice exhibit no evidence of glomerular or interstitial scarring, even at 9 months of age

increased urine protein level ( J:165315 )

• mice develop persistent proteinuria by 3 months of age

• rate of proteinuria increases modestly until 6 months and accelerates more rapidly thereafter

abnormal podocyte foot process morphology ( J:165315 )

• mice exhibit evidence of fine finger-like projections from the podocyte cell bodies and processes at 6 months of age

• foot process spreading is evident by 8 months of age

• following PS perfusion, foot processes exhibit a broadened and flattened morphology that is distinct from that in wild-type controls

podocyte microvillus transformation ( J:165315 )

• PS-treated podocytes develop unusually long fine processes that project from primary, secondary, and tertiary processes, suggesting pseudovillous transformation

• PS-treated mutant podocytes fail to recover normal morphology following subsequent infusion of heparin sulfate, unlike wild-type controls

integument

disheveled coat ( J:165315 )

• mice exhibit a scruffed appearance at 9 months of age

Allelic Composition	Cap1^tm1.1Mbrst/Cap1^tm1.1Mbrst Cfl1^tm1.1Wit/Cfl1^tm1.1Wit Tg(Nes-cre)1Kln/0
Genetic Background	involves: 129 * C57BL/6 * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cap1^tm1.1Mbrst mutation (0 available); any Cap1 mutation (32 available)
Cfl1^tm1.1Wit mutation (0 available); any Cfl1 mutation (25 available)
Tg(Nes-cre)1Kln mutation (4 available)

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

cellular

impaired neuron differentiation ( J:333563 )

• impaired growth cone morphology and motility

nervous system

impaired neuron differentiation ( J:333563 )

• impaired growth cone morphology and motility

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