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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Nes-cre)1Wme
transgene insertion 1, Werner Muller
MGI:2386545
Summary 14 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Atg7tm1Tchi/Atg7tm1Tchi
Sqstm1tm1Keta/Sqstm1tm1Keta
Tg(Nes-cre)1Wme/0
involves: 129 * C57BL/6 * C57BL/6NCrlj * CBA * CBA/JNCrlj MGI:3806624
cn2
Hif1antm1.1Rsjo/Hif1antm1.1Rsjo
Tg(Nes-cre)1Wme/0
involves: 129 * C57BL/6 * CBA MGI:4459909
cn3
Nbntm2Zqw/Nbntm2Zqw
Trp53tm1Brd/Trp53tm1Brd
Tg(Nes-cre)1Wme/0
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 * CBA MGI:3579669
cn4
Nbntm2Zqw/Nbntm2Zqw
Trp53tm1Brd/Trp53+
Tg(Nes-cre)1Wme/0
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 * CBA MGI:3579668
cn5
Juntm4Wag/Juntm4Wag
Tg(Nes-cre)1Wme/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:2451283
cn6
Gt(ROSA)26Sortm1(Trpv1,ECFP)Mde/Gt(ROSA)26Sor+
Tg(Nes-cre)1Wme/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3797083
cn7
Rbpjtm1Hon/Rbpjtm1Hon
Tg(Nes-cre)1Wme/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:2654079
cn8
Foxa2tm1Jrt/Foxa2tm1Khk
Tg(Nes-cre)1Wme/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3029694
cn9
Nbntm2Zqw/Nbntm2.1Zqw
Tg(Nes-cre)1Wme/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3579666
cn10
Nbntm2Zqw/Nbntm2Zqw
Tg(Nes-cre)1Wme/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3579667
cn11
Myh10tm7Rsad/Myh10tm7Rsad
Tg(Nes-cre)1Wme/0
involves: 129S6/SvEvTac * C57BL/6 * C57BL/6J * CBA MGI:4946094
cn12
Gt(ROSA)26Sortm1(CAG-Trp53*,-EGFP)Medz/Gt(ROSA)26Sor+
Tg(Nes-cre)1Wme/0
involves: C57BL/6 * CBA MGI:4443110
cn13
Atg7tm1Tchi/Atg7tm1Tchi
Tg(Nes-cre)1Wme/0
involves: C57BL/6 * CBA MGI:3806620
tg14
Tg(Nes-cre)1Wme/Tg(Nes-cre)1Wme involves: C57BL/6 * CBA MGI:6403910


Genotype
MGI:3806624
cn1
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
Sqstm1tm1Keta/Sqstm1tm1Keta
Tg(Nes-cre)1Wme/0
Genetic
Background
involves: 129 * C57BL/6 * C57BL/6NCrlj * CBA * CBA/JNCrlj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Sqstm1tm1Keta mutation (0 available); any Sqstm1 mutation (32 available)
Tg(Nes-cre)1Wme mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• large pyramidal neurons in the hippocampus are absent
• large pyramidal neurons in the cerebral cortex are absent
• Purkinje cells in the cerebellum are absent in these mice
• myelinated axons of the cerebellar nuclei are frequently enlarged and contain aberrant membranous structures and degenerated materials
• the cytoplasmic inclusion bodies containing ubiquitinated proteins that are found in the brain of Atg7 conditional knockouts are largely absent in these mice
• increased apoptosis of the neurons occurs in the cerebellar nucleus and the cerebral cortex

behavior/neurological
• abnormal limb clasping is observed in mice
• is observed

cellular
• increased apoptosis of the neurons occurs in the cerebellar nucleus and the cerebral cortex




Genotype
MGI:4459909
cn2
Allelic
Composition
Hif1antm1.1Rsjo/Hif1antm1.1Rsjo
Tg(Nes-cre)1Wme/0
Genetic
Background
involves: 129 * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1antm1.1Rsjo mutation (0 available); any Hif1an mutation (15 available)
Tg(Nes-cre)1Wme mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• decreased fasting plasma insulin levels

growth/size/body
• at 8 week and 10 week time points mice fed 60% fat diet gain significantly less weight




Genotype
MGI:3579669
cn3
Allelic
Composition
Nbntm2Zqw/Nbntm2Zqw
Trp53tm1Brd/Trp53tm1Brd
Tg(Nes-cre)1Wme/0
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nbntm2Zqw mutation (0 available); any Nbn mutation (59 available)
Tg(Nes-cre)1Wme mutation (1 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
N
• brain weight and cerebellar morphology are normal unlike in mutants with wild-type Trp53

behavior/neurological
N
• motor coordination defects seen in mutants with wild-type Trp53 are not seen in mutants that are homozygous null for Trp53

neoplasm
• similar to other Trp53 null mutations sarcomas and lymphomas are seen; however no cerebellar tumors have been detected




Genotype
MGI:3579668
cn4
Allelic
Composition
Nbntm2Zqw/Nbntm2Zqw
Trp53tm1Brd/Trp53+
Tg(Nes-cre)1Wme/0
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nbntm2Zqw mutation (0 available); any Nbn mutation (59 available)
Tg(Nes-cre)1Wme mutation (1 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• foliation structure is improved compared to mutants wild-type for Trp53
• a marginal increase in granule cell numbers is seen compared to mutants wild-type for Trp53

behavior/neurological
• performance on the balance beam test is improved compared to mutants wild-type for Trp53 but is impaired compared to controls and mutants that are homozygous null for Trp53




Genotype
MGI:2451283
cn5
Allelic
Composition
Juntm4Wag/Juntm4Wag
Tg(Nes-cre)1Wme/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Juntm4Wag mutation (0 available); any Jun mutation (12 available)
Tg(Nes-cre)1Wme mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 2% of animals survive to weaning
• animals born at less than the predicted Mendelian ratio

growth/size/body
• short body axis

skeleton
• fusion of neural arches

vision/eye
• severity of phenotype was variable




Genotype
MGI:3797083
cn6
Allelic
Composition
Gt(ROSA)26Sortm1(Trpv1,ECFP)Mde/Gt(ROSA)26Sor+
Tg(Nes-cre)1Wme/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(Trpv1,ECFP)Mde mutation (1 available); any Gt(ROSA)26Sor mutation (942 available)
Tg(Nes-cre)1Wme mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
N
• capsaicin infusion into striatum does not affect exploratory or motor behavior in Cre-activated mutants or controls
• infusion of capsaicin into striatum of results in stereotyped contralateral circling behavior within 5 minutes of delivery, while control mice without activation of Trpv1 show no effect

nervous system
• infusion of high doses of capsaicin (5-10 um) into striatum results in dose-dependent excitotoxicity in neuronal cultures
• at doses sufficient to induce circling, no cell death is observed
• in layer 5 cortical slices, capsaicin induces action potentials while cells from Cre-negative animals show no response
• neurons in slices show dose-dependent depolarizing currents in response to capsaicin applied to the bath
• capsaicin applied acutely to single cells causes reproducible bursts of action potentials with increases in firing rate; frequency of firing is dependent on duration and concentration of capsaicin application

homeostasis/metabolism
• infusion of high doses of capsaicin (5-10 um) into striatum results in dose-dependent excitotoxicity in neuronal cultures
• at doses sufficient to induce circling, no cell death is observed

cellular
• infusion of high doses of capsaicin (5-10 um) into striatum results in dose-dependent excitotoxicity in neuronal cultures
• at doses sufficient to induce circling, no cell death is observed




Genotype
MGI:2654079
cn7
Allelic
Composition
Rbpjtm1Hon/Rbpjtm1Hon
Tg(Nes-cre)1Wme/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rbpjtm1Hon mutation (2 available); any Rbpj mutation (193 available)
Tg(Nes-cre)1Wme mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• cysts result from aberrant fate determination of stem cells to epidermal progenitors and their accelerated differentiation into epidermis

integument
• cysts in the dermal layer but not in the epidermis, close to hair follicles, frequently in the vibrissa region
• cysts are composed of epidermal cells aberrantly differentiated from mutant hair follicular stem cells
• cyst formation occurs after hair loss or after the first hair cycle
• begin to lose hair 1-3 months after birth, when the first or second hair cycle terminates
• hair loss frequently occurs in the vibrissa region
• hyperkeratinization of the epidermis on the back and tail
• epidermis is thickened in some regions

growth/size/body
• cysts in the dermal layer but not in the epidermis, close to hair follicles, frequently in the vibrissa region
• cysts are composed of epidermal cells aberrantly differentiated from mutant hair follicular stem cells
• cyst formation occurs after hair loss or after the first hair cycle




Genotype
MGI:3029694
cn8
Allelic
Composition
Foxa2tm1Jrt/Foxa2tm1Khk
Tg(Nes-cre)1Wme/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxa2tm1Jrt mutation (2 available); any Foxa2 mutation (26 available)
Foxa2tm1Khk mutation (1 available); any Foxa2 mutation (26 available)
Tg(Nes-cre)1Wme mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

embryo
• the axial mesendoderm failed to differentiate; the anterior neural plate and anterior definitive endoderm form, but fail to maintain specification

nervous system
• anterior head truncations were noted in mutant animals




Genotype
MGI:3579666
cn9
Allelic
Composition
Nbntm2Zqw/Nbntm2.1Zqw
Tg(Nes-cre)1Wme/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nbntm2.1Zqw mutation (0 available); any Nbn mutation (59 available)
Nbntm2Zqw mutation (0 available); any Nbn mutation (59 available)
Tg(Nes-cre)1Wme mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• neural stem and progenitor cells from E13.5 brains produce fewer and smaller neurospheres in culture, do not produce secondary neurospheres, and have an increased number of chromosomal breaks per metaphase; however, no increase in apoptosis is seen
• no primary neurospheres were isolated from newborn mutants
• at E15.5, E18.5, and P7, proliferation of cells is decreased in the outer external granule cell layer
• at E15.5, E18.5, and P7, apoptosis is increased in the inner external granule cell layer
• seen at P7
• at P0 the Purkinje cell layer is disorganized
• at P0 the granule cell layer is disorganized with a reduction in the number of granule cells and ectopic presence of Purkinje cells
• seen at P7-P21
• at P0 the Bergmann glia are abnormal

behavior/neurological
• when suspended by the tail mutants stretch out their hind limbs
• seen after P7
• cerebellar ataxia seen after P7
• after P7 mutants are unable to complete the balance beam test
• seen after P7
• seen after P7
• increased repetitive movements seen after P7

growth/size/body
• detected by P7 and mutants reach only about half of the body weight of control mice at weaning

cellular
• neural stem and progenitor cells from E13.5 brains produce fewer and smaller neurospheres in culture, do not produce secondary neurospheres, and have an increased number of chromosomal breaks per metaphase; however, no increase in apoptosis is seen
• no primary neurospheres were isolated from newborn mutants




Genotype
MGI:3579667
cn10
Allelic
Composition
Nbntm2Zqw/Nbntm2Zqw
Tg(Nes-cre)1Wme/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nbntm2Zqw mutation (0 available); any Nbn mutation (59 available)
Tg(Nes-cre)1Wme mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• neural stem and progenitor cells from E13.5 brains produce fewer and smaller neurospheres in culture, do not produce secondary neurospheres, and have an increased number of chromosomal breaks per metaphase; however, no increase in apoptosis is seen
• no primary neurospheres were isolated from newborn mutants
• at E15.5, E18.5, and P7, proliferation of cells is decreased in the outer external granule cell layer
• at E15.5, E18.5, and P7, apoptosis is increased in the inner external granule cell layer
• seen at P7
• at P0 the Purkinje cell layer is disorganized
• seen at P7-P21
• at P0 the Bergmann glia are abnormal

behavior/neurological
• when suspended by the tail mutants stretch out their hind limbs
• seen after P7
• cerebellar ataxia seen after P7
• after P7 mutants are unable to complete the balance beam test
• seen after P7
• seen after P7
• increased repetitive movements seen after P7

growth/size/body
• detected by P7 and mutants reach only about half of the body weight of control mice at weaning

cellular
• no primary neurospheres were isolated from newborn mutants
• neural stem and progenitor cells from E13.5 brains produce fewer and smaller neurospheres in culture, do not produce secondary neurospheres, and have an increased number of chromosomal breaks per metaphase; however, no increase in apoptosis is seen




Genotype
MGI:4946094
cn11
Allelic
Composition
Myh10tm7Rsad/Myh10tm7Rsad
Tg(Nes-cre)1Wme/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6 * C57BL/6J * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Myh10tm7Rsad mutation (1 available); any Myh10 mutation (95 available)
Tg(Nes-cre)1Wme mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die between P12 and P22

nervous system
• severe
• paper-thin with the absence of most brain cortical tissue
• at P7, the spinal canal is ablated unlike in wild-type mice

behavior/neurological

cardiovascular system
N
• unlike null mice, cardiac development is normal




Genotype
MGI:4443110
cn12
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-Trp53*,-EGFP)Medz/Gt(ROSA)26Sor+
Tg(Nes-cre)1Wme/0
Genetic
Background
involves: C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(CAG-Trp53*,-EGFP)Medz mutation (1 available); any Gt(ROSA)26Sor mutation (942 available)
Tg(Nes-cre)1Wme mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
N
• hematopoietic stem and progenitor cells of irradiated mice treated with tamoxifen do not exhibit a selective advantage over cells not expressing the modified cDNA
• following irradiation, the proportion of GFP+ cells in the hematopoietic stem and progenitor cell compartment and myeloid and lymphoid lineages of tamoxifen-treated mice is increased compared to un-irradiated mice




Genotype
MGI:3806620
cn13
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
Tg(Nes-cre)1Wme/0
Genetic
Background
involves: C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Tg(Nes-cre)1Wme mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• the neurons of the cerebral cortex have defects in autophagy leading to a build up of cytoplasmic inclusion bodies that contain ubiquitinated proteins
• these inclusion bodies are visible two days after birth and grow in size and number during development
• increased apoptosis of the neurons occurs in the cerebellar nucleus and the cerebral cortex

homeostasis/metabolism
• the neurons of the cerebral cortex have defects in autophagy leading to a build up of cytoplasmic inclusion bodies that contain ubiquitinated proteins
• these inclusion bodies are visible two days after birth and grow in size and number during development

nervous system
• large pyramidal neurons in the hippocampus are absent
• large pyramidal neurons in the cerebral cortex are absent
• myelinated axons of the cerebellar nuclei are frequently enlarged and contain aberrant membranous structures and degenerated material
• the neurons of the cerebral cortex have defects in autophagy leading to a build up of cytoplasmic inclusion bodies that contain ubiquitinated proteins
• these inclusion bodies are visible two days after birth and grow in size and number during development
• increased apoptosis of the neurons occurs in the cerebellar nucleus and the cerebral cortex

behavior/neurological
• abnormal limb clasping is observed in mice
• is observed




Genotype
MGI:6403910
tg14
Allelic
Composition
Tg(Nes-cre)1Wme/Tg(Nes-cre)1Wme
Genetic
Background
involves: C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Nes-cre)1Wme mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all mice die within 5 weeks

nervous system
• in the developing cortex and cerebellum at E19.5 and P2
• fewer reach the cortical plate
• in all mice within the first month of age
• secondary to the reduction in neural progenitors
• at P2
• in all mice within the first month of age
• at E19.5, the area occupied by the ventricle is 8-fold compared with wild-type mice
• small and disorganized
• thin with disorganized layers at P8
• however, no defects are observed in the choroid plexus
• severely at P8
• underdeveloped
• loss and disorganization of myelinated axons at P18
• in the cortex

growth/size/body

behavior/neurological

cellular
• in the brain of E12.5 embryo
• in the developing cortex and cerebellum at E19.5 and P2
• fewer reach the cortical plate





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last database update
04/16/2024
MGI 6.23
The Jackson Laboratory