Phenotypes associated with this allele

• Allele Symbol: Rhob^tm1Gcp
• Allele Name: targeted mutation 1, George C Prendergast
• Allele ID: MGI:2387429
• Summary: 3 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Rhob^tm1Gcp/Rhob^tm1Gcp	involves: 129	MGI:2655505
hm2	Rhob^tm1Gcp/Rhob^tm1Gcp	Not Specified	MGI:2680037
cx3	Myo9a^tm1.2Bah/Myo9a^tm1.2Bah Rhob^tm1Gcp/Rhob^tm1Gcp	involves: 129/Sv * C57BL/6 * SJL	MGI:6120522

Genotype
MGI:2655505

hm1

• Allelic Composition: Rhob^tm1Gcp/Rhob^tm1Gcp
• Genetic Background: involves: 129

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

neoplasm

increased incidence of induced tumors ( J:71577 )

• upon necropsy 2 weeks after injection of neoplastically (E1A-plus-Ras-) transformed cells into the peritoneal cavity of female 129/Sv syngeneic mice, homozygous mutant cells yield an increased number of tumor nodules relative to heterozygous mutant cells

increased incidence of tumors by chemical induction ( J:71577 )

• in a model of DMBA-induced skin tumorigenesis, homozygotes develop a higher number of benign skin papillomas than heterozygotes, with no significant differences in tumor size or in susceptibility to carcinoma formation over a 16 week observation period

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:71577 )

N • homozygotes appear developmentally normal and do not display any defects in wound healing relative to wild-type littermates

increased incidence of tumors by chemical induction ( J:71577 )

• in a model of DMBA-induced skin tumorigenesis, homozygotes develop a higher number of benign skin papillomas than heterozygotes, with no significant differences in tumor size or in susceptibility to carcinoma formation over a 16 week observation period

cellular

abnormal cell physiology ( J:71577 )

• neoplastically (E1A-plus-Ras-) transformed mutant MEFs display altered actin and proliferative responses to TGFbeta

abnormal cell adhesion ( J:71577 )

• unlike primary mutant MEFs, neoplastically (E1A-plus-Ras-) transformed mutant MEFs show a significant reduction in the rate of substratum attachment and spreading on fibronectin

decreased fibroblast cell migration ( J:71577 )

• primary MEFs derived from homozygous mutant embryos show defective motility on fibronectin, as determined by the rate at which cells move into a cleared section of a confluent monolayer in the presence of the cell division inhibitor mitomycin C

• defective motility on fibronectin is associated with an altered gel mobility of the 1 integrin fibronectin receptor subunit in mutant MEFs

• however, cell adhesion and spreading appear unaffected, and no motility defects are observed during the healing of various types of skin wounds generated in mutant mice

Genotype
MGI:2680037

hm2

• Allelic Composition: Rhob^tm1Gcp/Rhob^tm1Gcp
• Genetic Background: Not Specified

growth/size/body

decreased body size ( J:86323 )

• homozygotes are noticeably smaller than wild-type and heterozygous littermates

vision/eye

abnormal retina vasculature morphology ( J:86323 )

• newborn homozygotes display a delay in the outgrowth of the primary vascular plexus in the retina consistent with impaired capillary sprouting

• at P4, sprouting vessels have not yet formed a capillary plexus and are only just beginning to expand from the optic disc covering only 30%-40% of the area covered in wild-type mice

• at P4, mutant blood vessel tips are morphologically abnormal and lack the characteristic cytoplasmic extensions observed in wild-type vessels

• in contrast, the neural portions of the retina and other parts of the eye, including the lens and cornea, appear normal in structure and cellularity

cardiovascular system

abnormal retina vasculature morphology ( J:86323 )

• newborn homozygotes display a delay in the outgrowth of the primary vascular plexus in the retina consistent with impaired capillary sprouting

• at P4, sprouting vessels have not yet formed a capillary plexus and are only just beginning to expand from the optic disc covering only 30%-40% of the area covered in wild-type mice

• at P4, mutant blood vessel tips are morphologically abnormal and lack the characteristic cytoplasmic extensions observed in wild-type vessels

• in contrast, the neural portions of the retina and other parts of the eye, including the lens and cornea, appear normal in structure and cellularity

abnormal vascular development ( J:86323 )

• newborn homozygotes exhibit retarded vascular development characterized by abnormal sprout morphology in the retina

Genotype
MGI:6120522

cx3

• Allelic Composition: Myo9a^tm1.2Bah/Myo9a^tm1.2Bah; Rhob^tm1Gcp/Rhob^tm1Gcp
• Genetic Background: involves: 129/Sv * C57BL/6 * SJL

nervous system

abnormal cerebral aqueduct morphology ( J:251454 )

• stenosis by P21.5