Analysis Tools
nervous system
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• some mice exhibit ventral-temporal (VT) retinal ganglion cell axon mapping defects compared with control mice
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Allele Symbol Allele Name Allele ID |
Ephb3tm1Kln targeted mutation 1, Rudiger Klein MGI:2149669 |
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| Summary |
20 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• some mice exhibit ventral-temporal (VT) retinal ganglion cell axon mapping defects compared with control mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mossy fiber pruning is defective
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• infra-pyramidal bundle (IPB) axons are longer than in wild-type mice
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| N |
• on a predominantly CD-1 or 129 genetic background, none of the adult homozygotes exhibit a circling phenotype
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• mossy fiber pruning is defective
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• an increased incidence of hypospadia compared to Efnb2tm1Henk heterozygotes is seen
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• the perineal area is reduced
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• hypospadia similar to that seen in Efnb2tm1Henk heterozygotes is seen
• hypospadia is not seen in either single homozygote
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• the perineal area is reduced
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• unlike in
Ephb2tm2Paw
Ephb3tm1Kln double mutants, Paneth cell positioning is normal
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• reduction in the number of mitotic cells in intestinal crypts was indistinguishable from unlike in
Ephb2tm3.1Jf
Ephb3tm1Kln double mutants
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• unlike in
Ephb2tm2Paw
Ephb3tm1Kln double mutants, Paneth cell positioning is normal
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• the number of mitotic cells in intestinal crypts was reduced to a similar extent as in
Ephb2tm2Paw
Ephb3tm1Kln double mutants
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• the number of mitotic cells in intestinal crypts was reduced to a similar extent as in
Ephb2tm2Paw
Ephb3tm1Kln double mutants
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• some mice exhibit ventral-temporal (VT) retinal ganglion cell axon mapping defects compared with control mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• Background Sensitivity: failure of midline closure of the abdominal wall resembling omphalocele in 39% of mice on a 129 background but not in mice on a CD-1 background
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• some mice exhibit ventral-temporal (VT) retinal ganglion cell axon mapping defects compared with control mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• some mice exhibit ventral-temporal (VT) retinal ganglion cell axon mapping defects compared with control mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• some mice exhibit ventral-temporal (VT) retinal ganglion cell axon mapping defects compared with control mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• some mice exhibit ventral-temporal (VT) retinal ganglion cell axon mapping defects compared with control mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• some mice exhibit ventral-temporal (VT) retinal ganglion cell axon mapping defects compared with control mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• Background Sensitivity: failure of midline closure of the abdominal wall resembling omphalocele in 9% of mice on a 129 background but not in mice on a CD-1 background
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• on a predominantly CD-1 background, only 18% of the expected double homozygotes survive to adulthood
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• on a predominantly CD-1 background (5 to 9 backcross generations), 91% of double homozygotes that survive to adulthood exhibit circling
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• at E13.5, double homozygotes show delayed outgrowth of efferent projections into both the ipsilateral and contralateral inner ears
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• at E13.5, both ipsilateral and contralateral projections of inner ear efferent (IEE) axons are disoriented and exhibit a temporary difficulty in reaching their targets
• as a result, ectopic caudal extensions are formed at the midline of the hindbrain with a 1- to 2-day delay in arriving at the ear end organs
• at E14.5 or later, axon tracing of IEEs shows a fairly normal number of crossed and uncrossed fibers in mutant mice
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• at E13.5, double homozygotes display delayed growth of efferent projections into both the ipsilateral and contralateral inner ears
• at this stage, growth cones have not yet reached into the sensory epithelia of the semicircular canals and there is an aberrant pausity of axons destined for the saccule and utricle
• in contrast, growth of afferent projections into the inner ear are normal, with afferents reaching all sensory epithelia by E12.5
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• all adult circling mutants display much thinner semicircular canals (SCCs), with a significantly reduced (5-fold) cross-sectional diameter, esp. in the anterior vertical SCC
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• at P7, the endolymph-filled membranous ducts are severely reduced by 53-fold in accord with a collapsed lumen and deflated SCCs
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• on a CD-1 background, reduced endolymph-filled lumens lead to a significant reduction in the flow of endolymph fluid through the semicircular canals
• [K+] is significantly reduced from a mean of 118 mM in wild-type mice to 29 mM in double homozygotes
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• on a CD-1 background, transepithelial utricular potential (UP) of the vestibular endolymph is significantly reduced from a mean of 0.4 mV in wild-type mice to -14.0 mV in double homozygotes
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• on a CD-1 background, double homozygotes fail to properly regulate the ionic homeostasis of vestibular endolymph
• however, blood hematocrit, [K+], and osmolarity appear to be nomal
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• severe vestibular dysfunction is associated with a drastic reduction in the volume of endolymph fluid within the vestibular apparatus
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• severe cleft palate in 41% of mice at E18.5
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• about a 50% decrease in the number of proliferating cells is seen in the colon; however, no change in the number of apoptotic cells is seen and the number of proliferating cells in small intestinal crypts is similar to wild-type
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• in the small intestine Paneth cells are displaced from the base of the crypts by proliferating cells while the number of proliferating cells in the normal progenitor niche (along the sides of the crypt) are reduced
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• differentiated Paneth cells are mispositioned and spread throughout the crypt-villus axis
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• decrease in proliferation in colon crypts
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• about a 50% decrease in the number of proliferating cells is seen in the colon; however, no change in the number of apoptotic cells is seen and the number of proliferating cells in small intestinal crypts is similar to wild-type
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• in the small intestine Paneth cells are displaced from the base of the crypts by proliferating cells while the number of proliferating cells in the normal progenitor niche (along the sides of the crypt) are reduced
|
|
• differentiated Paneth cells are mispositioned and spread throughout the crypt-villus axis
|
|
• severe cleft palate in 41% of mice at E18.5
|
|
• at E13.5, double homozygotes show delayed outgrowth of efferent projections into both the ipsilateral and contralateral inner ears
|
|
• at E13.5, both ipsilateral and contralateral projections of inner ear efferent (IEE) axons are disoriented and exhibit a temporary difficulty in reaching their targets
• as a result, ectopic caudal extensions are formed at the midline of the hindbrain with a 1- to 2-day delay in arriving at the ear end organs
• at E14.5 or later, axon tracing of IEEs shows a fairly normal number of crossed and uncrossed fibers in mutant mice
|
|
• severe cleft palate in 41% of mice at E18.5
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mossy fiber pruning is defective
|
|
• infra-pyramidal bundle (IPB) axons are longer than in wild-type mice
|
|
• mossy fiber pruning is defective
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• Background Sensitivity: on a predominantly CD-1 background, 45% of the expected double homozygotes survive as adults whereas only 6% of the expected double homozygotes survive as adults on a 129 background
|
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• Background Sensitivity: on a predominantly CD-1 background (5 to 9 backcross generations), 100% of double homozygotes that survive to adulthood exhibit circling; in contrast, none of the small number of 129 double homozygotes that survive to adulthood circle
• cicling is first evident when pups are old enough to walk and continues into adulthood
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• at E13.5, double homozygotes show delayed outgrowth of efferent projections into both the ipsilateral and contralateral inner ears
|
|
• at E13.5, both ipsilateral and contralateral projections of inner ear efferent (IEE) axons are disoriented and exhibit a temporary difficulty in reaching their targets
• as a result, ectopic caudal extensions are formed at the midline of the hindbrain with a 1- to 2-day delay in arriving at the ear end organs
• at E14.5 or later, axon tracing of IEEs shows a fairly normal number of crossed and uncrossed fibers in mutant mice
|
|
• at E13.5, double homozygotes display delayed growth of efferent projections into both the ipsilateral and contralateral inner ears
• at this stage, growth cones have not yet reached into the sensory epithelia of the semicircular canals and there is an aberrant pausity of axons destined for the saccule and utricle
• in contrast, growth of afferent projections into the inner ear are normal, with afferents reaching all sensory epithelia by E12.5
|
|
• all adult circling mutants display much thinner semicircular canals (SCCs), with a significantly reduced (5-fold) cross-sectional diameter, esp. in the anterior vertical SCC
|
|
• at P21, circling double homozygotes display loosely associated basolateral membranes in vestibular dark cells as well as severe extracellular edema
• in addition, the apical surface of dark cells facing the endolymph-filled lumen shows an accumulation of fluid-filled vesicles
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|
• at P7, the endolymph-filled membranous ducts are severely reduced by 53-fold in accord with a collapsed lumen and deflated SCCs
|
|
• on a CD-1 background, reduced endolymph-filled lumens lead to a significant reduction in the flow of endolymph fluid through the semicircular canals
• [K+] is significantly reduced from a mean of 118 mM in wild-type mice to 29 mM in double homozygotes
|
|
• on a CD-1 background, transepithelial utricular potential (UP) of the vestibular endolymph is significantly reduced from a mean of 0.4 mV in wild-type mice to -14.0 mV in double homozygotes
|
|
• on a CD-1 background, double homozygotes fail to properly regulate the ionic homeostasis of vestibular endolymph
• however, blood hematocrit, [K+], and osmolarity appear to be nomal
|
|
• severe vestibular dysfunction is associated with a drastic reduction in the volume of endolymph fluid within the vestibular apparatus
|
|
• severe cleft palate in 15% of mice at E18.5
|
|
• about a 50% decrease in the number of proliferating cells is seen in the colon; however, no change in the number of apoptotic cells is seen
|
|
• in the small intestine Paneth cells are displaced from the base of the crypts by proliferating cells while the number of proliferating cells in the normal progenitor niche (along the sides of the crypt) are reduced
|
|
• about a 50% decrease in the number of proliferating cells is seen in the colon; however, no change in the number of apoptotic cells is seen
|
|
• in the small intestine Paneth cells are displaced from the base of the crypts by proliferating cells while the number of proliferating cells in the normal progenitor niche (along the sides of the crypt) are reduced
|
|
• severe cleft palate in 15% of mice at E18.5
|
|
• at E13.5, double homozygotes show delayed outgrowth of efferent projections into both the ipsilateral and contralateral inner ears
|
|
• at E13.5, both ipsilateral and contralateral projections of inner ear efferent (IEE) axons are disoriented and exhibit a temporary difficulty in reaching their targets
• as a result, ectopic caudal extensions are formed at the midline of the hindbrain with a 1- to 2-day delay in arriving at the ear end organs
• at E14.5 or later, axon tracing of IEEs shows a fairly normal number of crossed and uncrossed fibers in mutant mice
|
|
• severe cleft palate in 15% of mice at E18.5
|
|
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• cell proliferation and Paneth cell displacement are normal
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• axons from ventrotemporal retina tend to cross the midline
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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 05/14/2024 MGI 6.23 |
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