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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Nes-cre)1Kag
transgene insertion 1, Ryoichiro Kageyama
MGI:2176222
Summary 13 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Hprt1tm1(CAG-Gys1*)Jjg/?
Tg(Nes-cre)1Kag/?
involves: 129P2/OlaHsd MGI:5697674
cn2
Mapk1tm1.2Kuta/Mapk1tm1.2Kuta
Tg(Nes-cre)1Kag/0
involves: 129P2/OlaHsd * C57BL/6J MGI:5293439
cn3
Abl1tm1Ajk/Abl1tm1Ajk
Abl2tm1Ajk/Abl2tm1Ajk
Tg(Nes-cre)1Kag/?
involves: 129S4/SvJae MGI:3583883
cn4
Huwe1tm1Alas/Y
Tg(Nes-cre)1Kag/0
involves: 129S7/SvEvBrd MGI:4821353
cn5
Dmrta2tm1.1Fuma/Dmrta2tm1.1Fuma
Tg(Nes-cre)1Kag/0
involves: C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj * SJL MGI:5527534
cn6
Spentm2.1Hon/Spentm2.1Hon
Tg(Nes-cre)1Kag/?
involves: C57BL/6 * CBA MGI:3710557
cn7
Sqstm1tm1.1Ewa/Sqstm1tm1.1Ewa
Tg(Nes-cre)1Kag/0
involves: C57BL/6J MGI:5547387
cn8
Nhlrc1tm1(KOMP)Vlcg/Nhlrc1tm1(KOMP)Vlcg
Gys1tm1c(EUCOMM)Wtsi/Gys1+
Tg(Nes-cre)1Kag/?
involves: C57BL/6NTac MGI:5697671
cn9
Nhlrc1tm1(KOMP)Vlcg/Nhlrc1tm1(KOMP)Vlcg
Gys1tm1c(EUCOMM)Wtsi/Gys1tm1c(EUCOMM)Wtsi
Tg(Nes-cre)1Kag/?
involves: C57BL/6NTac MGI:5697670
cn10
Wasltm1.1Ttha/Wasltm1.1Ttha
Tg(Nes-cre)1Kag/0
involves: C57BL/6 * SJL MGI:5662272
cn11
Wasltm1.1Ttha/Wasl+
Tg(Nes-cre)1Kag/0
involves: C57BL/6 * SJL MGI:5662273
cn12
Hif1atm1Stom/Hif1atm1.1Stom
Tg(Nes-cre)1Kag/0
Not Specified MGI:3815314
cn13
Setdb1tm1.1Yshk/Setdb1tm1.1Yshk
Tg(Nes-cre)1Kag/0
Not Specified MGI:5440723


Genotype
MGI:5697674
cn1
Allelic
Composition
Hprt1tm1(CAG-Gys1*)Jjg/?
Tg(Nes-cre)1Kag/?
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hprt1tm1(CAG-Gys1*)Jjg mutation (0 available); any Hprt1 mutation (1274 available)
Tg(Nes-cre)1Kag mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• extensive brain accumulation of glycogen

cellular

nervous system
• extensive brain accumulation of glycogen




Genotype
MGI:5293439
cn2
Allelic
Composition
Mapk1tm1.2Kuta/Mapk1tm1.2Kuta
Tg(Nes-cre)1Kag/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mapk1tm1.2Kuta mutation (0 available); any Mapk1 mutation (40 available)
Tg(Nes-cre)1Kag mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• context freezing response is significantly reduced
• cued fear conditioning response is reduced after a 48 h retention delay
• resident males show a shorter latency to attack and attack for a longer duration with a higher frequency
• spend more time in the center of an open field and spend more time in the open arms of a plus maze compared to controls
• fail to show a preference for a novel mouse
• decrease in interaction with a novel object compared to controls
• pups are more scattered in the home cage
• show a significantly shorter duration of crouching to keep the pups warm and to nurse them
• show little nest building activity and build shallower nest compared to controls
• males display persistent interest when presented with the same female indicating a failure to develop social memory
• fail to show a preference for a novel mouse
• in an open field test for social versus inanimate preference, mice show no significant difference in time spent interacting with the social or inanimate targets unlike controls
• in a sociability test for social versus empty preference, mice show a significant decrease in interaction with the social target compared to controls

nervous system
• in the cortices at 13 weeks of age

taste/olfaction
N
• no defect in olfaction is detected

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
autism spectrum disorder DOID:0060041 J:176051




Genotype
MGI:3583883
cn3
Allelic
Composition
Abl1tm1Ajk/Abl1tm1Ajk
Abl2tm1Ajk/Abl2tm1Ajk
Tg(Nes-cre)1Kag/?
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Abl1tm1Ajk mutation (1 available); any Abl1 mutation (92 available)
Abl2tm1Ajk mutation (0 available); any Abl2 mutation (79 available)
Tg(Nes-cre)1Kag mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• only 35% of the expected Mendelian numbers are born
• those that were born survived well into adulthood

nervous system
• smaller dendrite arbors resulting in more densely packed neurons in all layers of cortex in 6-8 weeks old mice




Genotype
MGI:4821353
cn4
Allelic
Composition
Huwe1tm1Alas/Y
Tg(Nes-cre)1Kag/0
Genetic
Background
involves: 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Huwe1tm1Alas mutation (0 available); any Huwe1 mutation (63 available)
Tg(Nes-cre)1Kag mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

nervous system
• at E13.5, E15.5, E18.5, fewer progenitors exit the cell cycle compared with wild-type mice
• at E18.5, proliferation of neuronal precursors is increased compared to in wild-type mice
• at E18.5, the length of the cycle is lengthened compared to in wild-type cells
• brains contain ectopic cellular clusters in differentiated striatal regions unlike in wild-type mice
• however, no abnormalities are observed at E15.5
• the cortex exhibits an increase in cellular density and decrease in intervening neuropil compared to in wild-type mice
• laminar organization is altered with no clearly identifiable superficial neuron layers compared to in wild-type mice
• very small
• in the germinal layers

cellular
• at E13.5, E15.5, E18.5, fewer progenitors exit the cell cycle compared with wild-type mice
• at E18.5, proliferation of neuronal precursors is increased compared to in wild-type mice
• at E18.5, the length of the cycle is lengthened compared to in wild-type cells




Genotype
MGI:5527534
cn5
Allelic
Composition
Dmrta2tm1.1Fuma/Dmrta2tm1.1Fuma
Tg(Nes-cre)1Kag/0
Genetic
Background
involves: C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dmrta2tm1.1Fuma mutation (0 available); any Dmrta2 mutation (15 available)
Tg(Nes-cre)1Kag mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
N
• mice exhibit normal formation of the cortical hem and the hippocampal primordium in the medial cortex
• moderate at E15.5
• however, size is normal at E12.5




Genotype
MGI:3710557
cn6
Allelic
Composition
Spentm2.1Hon/Spentm2.1Hon
Tg(Nes-cre)1Kag/?
Genetic
Background
involves: C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Spentm2.1Hon mutation (3 available); any Spen mutation (140 available)
Tg(Nes-cre)1Kag mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• increased mortality before 10 weeks of age

growth/size/body
• although normal at birth, mice are growth retarded at 3 weeks of age

nervous system
• reduced in size
• severe reductions in the thickness of the cerebral cortex




Genotype
MGI:5547387
cn7
Allelic
Composition
Sqstm1tm1.1Ewa/Sqstm1tm1.1Ewa
Tg(Nes-cre)1Kag/0
Genetic
Background
involves: C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sqstm1tm1.1Ewa mutation (0 available); any Sqstm1 mutation (32 available)
Tg(Nes-cre)1Kag mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• body weight gradually increases after 20 weeks of age, becoming significantly greater than littermate controls by 27 weeks of age

adipose tissue
• increase in visceral fat

behavior/neurological




Genotype
MGI:5697671
cn8
Allelic
Composition
Nhlrc1tm1(KOMP)Vlcg/Nhlrc1tm1(KOMP)Vlcg
Gys1tm1c(EUCOMM)Wtsi/Gys1+
Tg(Nes-cre)1Kag/?
Genetic
Background
involves: C57BL/6NTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gys1tm1c(EUCOMM)Wtsi mutation (0 available); any Gys1 mutation (56 available)
Nhlrc1tm1(KOMP)Vlcg mutation (0 available); any Nhlrc1 mutation (14 available)
Tg(Nes-cre)1Kag mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• reduced induction of seizures by Kainic acid
• modest seizure response following train stimulation of CA3-CA1 synapse
• modest neurodegeneration in brains

cellular
• modest level of autophagy

behavior/neurological
• reduced induction of seizures by Kainic acid
• modest seizure response following train stimulation of CA3-CA1 synapse

homeostasis/metabolism
• modest level of autophagy




Genotype
MGI:5697670
cn9
Allelic
Composition
Nhlrc1tm1(KOMP)Vlcg/Nhlrc1tm1(KOMP)Vlcg
Gys1tm1c(EUCOMM)Wtsi/Gys1tm1c(EUCOMM)Wtsi
Tg(Nes-cre)1Kag/?
Genetic
Background
involves: C57BL/6NTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gys1tm1c(EUCOMM)Wtsi mutation (0 available); any Gys1 mutation (56 available)
Nhlrc1tm1(KOMP)Vlcg mutation (0 available); any Nhlrc1 mutation (14 available)
Tg(Nes-cre)1Kag mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
N
• no neurodegeneration in brains
• reduced induction of seizures by Kainic acid
• modest seizure response following train stimulation of CA3-CA1 synapse

cellular
N
• autophagy is not impaired

behavior/neurological
• reduced induction of seizures by Kainic acid
• modest seizure response following train stimulation of CA3-CA1 synapse




Genotype
MGI:5662272
cn10
Allelic
Composition
Wasltm1.1Ttha/Wasltm1.1Ttha
Tg(Nes-cre)1Kag/0
Genetic
Background
involves: C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Nes-cre)1Kag mutation (0 available)
Wasltm1.1Ttha mutation (0 available); any Wasl mutation (39 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice are born phenotypically normal with a near-Mendelian incidence (30% vs. 25% expected); however, all mice die prior to weaning within 3 to 4 weeks after birth (P18-P24)

growth/size/body
• at P7, P10 and P13, mice show a significant reduction in average body weight relative to controls
• by P5-P7, mice exhibit noticeably retarded growth rates relative to controls

behavior/neurological
• at P15, mice exhibit locomotor disturbance with lethargic pace
• at P15, mice exhibit broad-base stance/gait pattern

nervous system
• at P15, mice show a marked decrease in brain vascularization relative to controls
• at P15, an unusually large amount of cerebrospinal fluid (CSF) is drained out from the mutant skull during brain isolation
• CSF accumulation in the skull results in brain swelling and enlarged brain hemispheres
• hydrocephalus is likely caused by a blocked connection between the third and fourth ventricles
• the rostral segment of the aqueduct of Sylvius is abnormally narrow or completely collapsed
• at P15, mutant brains are noticeably larger than control brains
• hydrocephalic mice show major defects in the ependymal layer accompanied by a severe denudation of ependymal layers lining the ventricular wall
• N-cadherin immune-staining confirmed defects in ependymal layer integrity
• at P14-18, immunostaining with anti-acetylated tubulin revealed a severe reduction or absence of ependymal cilia in the lateral ventricles
• SEM micrographs confirmed that the surface of ependymal cells lining the lateral ventricles is relatively smooth and lacks the numerous fine projections seen in controls
• at 3 weeks of age, hydrocephalic mice show markedly enlarged ventricles in both anterior and posterior regions of lateral ventricles
• in hydrocephalic mice, dilation of the fourth ventricle is observed
• at 3 weeks of age, H&E-stained coronal brain sections revealed visibly dilated lateral ventricles along their entire rostrocaudal aspect
• in hydrocephalic mice, the choroid plexus displays an undefined border with disrupted cell alignment between adjacent cells
• an enlarged lumen is noted in the caudal part of the aqueduct
• in hydrocephalic mice, a unique type of columnar cells is absent in the rostral aqueduct wall due to aqueduct atresia and stenosis
• abnormal multilayered stratification of the ependymal cells lining along the caudal part of the aqueduct wall and increased cell numbers in the periaqueductal gray regions are observed
• hydrocephalic mice show a profound reduction in the corpus callosum
• hydrocephalic mice show a profound reduction in the caudate putamen
• strikingly, hydrocephalic mice show absence of hippocampal formation
• the spatial alignment and relation of cortical cell orientation are disrupted and compressed by the enlargement of the ventricle system
• however, no significant morphological deterioration is noted in anterior regions of the frontal cortex
• hydrocephalic brains exhibit reduced thickness of the cerebral cortex along its rostral and caudal parts
• hydrocephalic mice show a profound reduction in the cortical layers and septum
• Ki-67 staining revealed a significant decrease in cell proliferation in the subventricular zone relative to control mice
• GFAP staining revealed a marked increase in astrocyte density in the cerebral cortex and surrounding areas of the lateral ventricular regions, indicating astrogliosis
• mutant astrocytes tend to have an enlarged cell body and thicker processes than control astrocytes

skeleton
• at ~P10, mice develop a dome shaped skull morphology that becomes more prominent by P15
• at P15, mice display abnormal curvature of the thoracic vertebrae
• at P15, mice exhibit a hunchback body posture

craniofacial
• at ~P10, mice develop a dome shaped skull morphology that becomes more prominent by P15

cardiovascular system
• at P15, mice show a marked decrease in brain vascularization relative to controls

cellular
• at P14-18, immunostaining with anti-acetylated tubulin revealed a severe reduction or absence of ependymal cilia in the lateral ventricles
• SEM micrographs confirmed that the surface of ependymal cells lining the lateral ventricles is relatively smooth and lacks the numerous fine projections seen in controls




Genotype
MGI:5662273
cn11
Allelic
Composition
Wasltm1.1Ttha/Wasl+
Tg(Nes-cre)1Kag/0
Genetic
Background
involves: C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Nes-cre)1Kag mutation (0 available)
Wasltm1.1Ttha mutation (0 available); any Wasl mutation (39 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• mice have a normal life span and display no obvious defects in external morphology, weight, reproductive vigor, or behavior relative to wild-type controls




Genotype
MGI:3815314
cn12
Allelic
Composition
Hif1atm1Stom/Hif1atm1.1Stom
Tg(Nes-cre)1Kag/0
Genetic
Background
Not Specified
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1atm1.1Stom mutation (0 available); any Hif1a mutation (48 available)
Hif1atm1Stom mutation (0 available); any Hif1a mutation (48 available)
Tg(Nes-cre)1Kag mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• density of blood vessels is reduced
• in adults
• thinner than in controls at E19
• dense nuclei found with a wavy architecture
• apoptotic neural and glial cells detected
• atrophy of the cerebral cortex in adults
• significant reduction of neurons at 10 weeks of age although six layered structure of the cortex is maintained
• 36% reduction of neurons at 10 weeks of age
• 36% loss of neurons in the perirhinal cortex at 10 weeks of age
• 12% reduction of neurons on the dorsal side

behavior/neurological
N
• spontaneous activity is normal
• significantly impaired memory consolidation after 4 days of testing using a radial maze task




Genotype
MGI:5440723
cn13
Allelic
Composition
Setdb1tm1.1Yshk/Setdb1tm1.1Yshk
Tg(Nes-cre)1Kag/0
Genetic
Background
Not Specified
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Setdb1tm1.1Yshk mutation (1 available); any Setdb1 mutation (56 available)
Tg(Nes-cre)1Kag mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• born alive but do not survive beyond P10

nervous system
• increase in the number of astrocytes in the cortex at E18.5





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last database update
04/23/2024
MGI 6.23
The Jackson Laboratory