Phenotypes associated with this allele

• Allele Symbol: Sema4d^tm1Kik
• Allele Name: targeted mutation 1, Hitoshi Kikutani
• Allele ID: MGI:3027762
• Summary: 5 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Sema4d^tm1Kik/Sema4d^tm1Kik	B6.129P2-Sema4d^tm1Kik	MGI:5807143
hm2	Sema4d^tm1Kik/Sema4d^tm1Kik	involves: 129P2/OlaHsd	MGI:3706340
hm3	Sema4d^tm1Kik/Sema4d^tm1Kik	involves: 129P2/OlaHsd * C57BL/6	MGI:3027786
cx4	Sema4b^Gt(RST235)Byg/Sema4b^Gt(RST235)Byg Sema4d^tm1Kik/Sema4d^tm1Kik Sema4g^tm1Kik/Sema4g^tm1Kik	B6.Cg-Sema4b^Gt(RST235)Byg Sema4d^tm1Kik Sema4g^tm1Kik	MGI:5807148
cx5	Sema4a^tm1Kik/Sema4a^tm1Kik Sema4d^tm1Kik/Sema4d^tm1Kik	involves: 129P2/OlaHsd	MGI:3706317

Genotype
MGI:5807143

hm1

• Allelic Composition: Sema4d^tm1Kik/Sema4d^tm1Kik
• Genetic Background: B6.129P2-Sema4d^tm1Kik

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

renal/urinary system

renal/urinary system phenotype ( J:221423 )

N • mice show normal kidney morphology and a normal response to kidney ischemia/reperfusion injury

Genotype
MGI:3706340

hm2

• Allelic Composition: Sema4d^tm1Kik/Sema4d^tm1Kik
• Genetic Background: involves: 129P2/OlaHsd

nervous system

nervous system phenotype ( J:119485 )

N • neither defects in the cerebellum nor ectopic granule cells are observed despite being a possible ligand for Plxnb2

Genotype
MGI:3027786

hm3

• Allelic Composition: Sema4d^tm1Kik/Sema4d^tm1Kik
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6

behavior/neurological

behavior/neurological phenotype ( J:66033 )

N • behavior was normal

cardiovascular system

cardiovascular system phenotype ( J:66033 )

N • Phenotype was normal in these tissues where Sema4d^tm1Kik interacts through plexin-B1 receptors rather than through CD72 receptors as in lymphoid tissue

hematopoietic system

decreased B cell proliferation ( J:66033 )

• cell proliferation was slower in vitro

increased B cell number ( J:66033 )

• increased numbers of CD23+B220+ B cells

decreased T cell number ( J:66033 )

• Il4 and Ifn-gamma T-cells reduced in numbers

decreased CD4-positive, alpha-beta T cell number ( J:66033 )

• reduced in numbers

abnormal B-1 B cell morphology ( J:66033 )

• B-1 cell development abnormality

decreased B-1a cell number ( J:66033 )

• considerable reduction in numbers of CD5+B220+ B cells

decreased spleen germinal center size ( J:66033 )

• germinal centers in the spleen were smaller and with fewer antigen specific IgG1 cells

abnormal immunoglobulin level ( J:66033 )

• impaired IgG1 response to T-cell dependent antigen but not to T-cell independent antigens

• no abnormalities in serum levels of the various Ig classes however

immune system

decreased B cell proliferation ( J:66033 )

• cell proliferation was slower in vitro

increased B cell number ( J:66033 )

• increased numbers of CD23+B220+ B cells

decreased T cell number ( J:66033 )

• Il4 and Ifn-gamma T-cells reduced in numbers

decreased CD4-positive, alpha-beta T cell number ( J:66033 )

• reduced in numbers

abnormal B-1 B cell morphology ( J:66033 )

• B-1 cell development abnormality

decreased B-1a cell number ( J:66033 )

• considerable reduction in numbers of CD5+B220+ B cells

decreased spleen germinal center size ( J:66033 )

• germinal centers in the spleen were smaller and with fewer antigen specific IgG1 cells

abnormal immunoglobulin level ( J:66033 )

• impaired IgG1 response to T-cell dependent antigen but not to T-cell independent antigens

• no abnormalities in serum levels of the various Ig classes however

renal/urinary system

renal/urinary system phenotype ( J:66033 )

N • Phenotype was normal in these tissues where Sema4d^tm1Kik interacts through plexin-B1 receptors rather than through CD72 receptors as in lymphoid tissue

nervous system

nervous system phenotype ( J:66033 )

N • Phenotype was normal in these tissues where Sema4d^tm1Kik interacts through plexin-B1 receptors rather than through CD72 receptors as in lymphoid tissue

cellular

decreased B cell proliferation ( J:66033 )

• cell proliferation was slower in vitro

Genotype
MGI:5807148

cx4

• Allelic Composition: Sema4b^{Gt(RST235)Byg}/Sema4b^{Gt(RST235)Byg}; Sema4d^tm1Kik/Sema4d^tm1Kik; Sema4g^tm1Kik/Sema4g^tm1Kik
• Genetic Background: B6.Cg-Sema4b^{Gt(RST235)Byg} Sema4d^tm1Kik Sema4g^tm1Kik

homeostasis/metabolism

increased susceptibility to kidney reperfusion injury ( J:221423 )

• following renal ischemia/reperfusion injury, mice exhibit misorganized, multi-layered tubular kidney epithelium compared to controls

• tubular defects after kidney injury are confined to the outer renal medulla

renal/urinary system

increased susceptibility to kidney reperfusion injury ( J:221423 )

• following renal ischemia/reperfusion injury, mice exhibit misorganized, multi-layered tubular kidney epithelium compared to controls

• tubular defects after kidney injury are confined to the outer renal medulla

abnormal renal tubule epithelium morphology ( J:221423 )

• following renal ischemia/reperfusion injury, mice exhibit misorganized, multi-layered tubular kidney epithelium compared to controls

• however, mice are viable and show no overt defects in kidney histology under normal conditions

Genotype
MGI:3706317

cx5

• Allelic Composition: Sema4a^tm1Kik/Sema4a^tm1Kik; Sema4d^tm1Kik/Sema4d^tm1Kik
• Genetic Background: involves: 129P2/OlaHsd

nervous system

nervous system phenotype ( J:119485 )

N • neither defects in the cerebellum nor ectopic granule cells are observed despite being possible ligands for Plxnb2