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Phenotypes Associated with This Genotype
Genotype
MGI:2175009
Allelic
Composition
Rettm1Cos/Rettm1Cos
Genetic
Background
involves: 129S/SvEv * MF1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rettm1Cos mutation (2 available); any Ret mutation (35 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
muscle
• failure of milk to progress from the stomach to the intestine (J:23852)

mortality/aging
• death occurred 16-24 hours after birth (J:23852)

cardiovascular system
N
• no gross abnormalities, the ventricles, atria, valves, aorta and pulmonary trunk showed no defects

digestive/alimentary system
• failure of milk to progress from the stomach to the intestine (J:23852)

renal/urinary system
• remaining kidney rudiments are dysplastic with few nephric elements (proximal and distal tubules, glomeruli, and vessels) and no recognizable medulla, cortex, or nephrogenic zone (J:23852)
• dysplastic (J:30389)
• absence of mature collecting ducts
• persistence of large regions of undifferentiated mesenchyme
• the metanephric mesenchyme did not condense by E11.5
• the metanephric mesenchyme underwent apoptosis at E12.5
• no recognizable nephrogenic zone
• rudimetary and are of similar size to the adrenal glands when present
• variable penetrance; kidneys are absent or rudimetary; both unilateral and bilateral effects were observed (J:23852)
• variable penetrance (J:30389)
• variable severity; some animals exhibited an absent ureter and kidney, while others exhibited blind ureters with no renal tissue (J:23852)
• sometimes absent or blind-ending (J:30389)
• reduced branching of the ureter
• sometimes absent (J:30389)
• sometimes blind-ending (J:30389)
• of those buds that entered the mesenchyme, the growth and branching was abnormal, if occuring at all
• when the uteric bud was present, growth was retarded
• in approximately half of the mutant embryos, the uteric bud failed to evaginate although a mesenchymal blastema and a Wollfian duct were present in metanephroi
• when the uteric bud was present, growth was retarded and either failed to enter the mesenchyme or was delayed; at E11.0, 8% of the mutant buds had entered the mesenchyme

respiratory system
• underdeveloped or collapsed lungs; likely a secondary effect of deficient amniotic fluid production by the kidneys

nervous system
• no neurons in the small or large intestine, esophagus or stomach (J:23852)
• neurons and glia were absent from the distal stomach, duodenum, small and large intestine, but not the esophagus or the proximal stomach as determined by TH, NF or MASH-1 immunoreactivity (J:30830)
• cardiac ganglion volume was 56% smaller than controls, due to a reduction in neuronal cell number
• in two of six hearts, the AV node, the AV bundle and the proximal bundle branches were devoid of cholinergic fibers
• occasionally larger than in controls
• absent as early as E12.5, while all other sympathetic ganglia were present

embryo
• the metanephric mesenchyme underwent apoptosis at E12.5
• mutant enteric crest cells were detected in the esophagus and proximal stomach, but not the rest of the gastrointestinal tract
• reduced numbers of mesonephric tubules were observed at E11.5

cellular
• the metanephric mesenchyme underwent apoptosis at E12.5
• mutant enteric crest cells were detected in the esophagus and proximal stomach, but not the rest of the gastrointestinal tract

homeostasis/metabolism
• deficient amniotic fluid production by the kidneys


Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB), Gene Ontology (GO)
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last database update
08/06/2019
MGI 6.14
The Jackson Laboratory