About   Help   FAQ
Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(KRT5-rtTA)1Glk
transgene insertion 1, Adam Glick
MGI:3575756
Summary 9 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Droshatm1Ghan/Droshatm1Ghan
Tg(KRT5-rtTA)1Glk/0
Tg(tetO-cre)1Jaw/0
involves: 129 * C57BL/6 * FVB/N MGI:5431582
cn2
Droshatm1Litt/Droshatm1Litt
Tg(KRT5-rtTA)1Glk/0
Tg(tetO-cre)1Jaw/0
involves: 129P2/OlaHsd * C57BL/6 * FVB/N MGI:5431584
cn3
Dicer1tm1Smr/Dicer1tm1Smr
Tg(KRT5-rtTA)1Glk/0
Tg(tetO-cre)1Jaw/0
involves: 129S7/SvEvBrd * C57BL/6 * FVB/N MGI:5431583
cx4
Tg(KRT5-rtTA)1Glk/0
Tg(tetO/CMV-Tslp)#Sfz/0
C.Cg-Tg(KRT5-rtTA)1Glk Tg(tetO/CMV-Tslp)#Sfz MGI:5317912
cx5
Tcrbtm1Mom/Tcrbtm1Mom
Tg(KRT5-rtTA)1Glk/0
Tg(tetO/CMV-Tslp)#Sfz/0
involves: 129P2/OlaHsd * C3H * C57BL/6 * FVB/N MGI:5317870
cx6
Tg(KRT5-rtTA)1Glk/0
Tg(tetO/CMV-Tslp)#Sfz/0
involves: C3H * C57BL/6 * FVB/N MGI:5317865
cx7
Tg(KRT5-rtTA)1Glk/0
Tg(tetO-Tfrc/EGFP/Ova)#Sfz/0
Tg(tetO/CMV-Tslp)#Sfz/0
involves: C3H * C57BL/6 * FVB/N MGI:5503059
cx8
Tg(KRT5-rtTA)1Glk/0
Tg(tetO-TGFB1*C223S*C225S)1Glk/0
involves: FVB/N MGI:3815535
cx9
Tg(KRT5-rtTA)1Glk/0
Tg(tetO-Tfrc/EGFP/Ova)#Sfz/0
involves: FVB/N MGI:5503058


Genotype
MGI:5431582
cn1
Allelic
Composition
Droshatm1Ghan/Droshatm1Ghan
Tg(KRT5-rtTA)1Glk/0
Tg(tetO-cre)1Jaw/0
Genetic
Background
involves: 129 * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Droshatm1Ghan mutation (0 available); any Drosha mutation (63 available)
Tg(KRT5-rtTA)1Glk mutation (0 available)
Tg(tetO-cre)1Jaw mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
• at P50 doxycycline-treated mice exhibit loss of bulge stem cells unlike in control mice
• however, bulge stem cells are present at P20 and P22

growth/size/body
• in doxycycline-treated mice




Genotype
MGI:5431584
cn2
Allelic
Composition
Droshatm1Litt/Droshatm1Litt
Tg(KRT5-rtTA)1Glk/0
Tg(tetO-cre)1Jaw/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Droshatm1Litt mutation (1 available); any Drosha mutation (63 available)
Tg(KRT5-rtTA)1Glk mutation (0 available)
Tg(tetO-cre)1Jaw mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
N
• doxycycline-treated mice retain hair follicle stem cells in early telogen and anagen
• hair phenotype in doxycycline-treated mice appears more slowly than in Dicer1tm1Smr/Dicer1tm1Smr Tg(KRT5-rtTA)1Glk Tg(tetO-cre)1Jaw mice
• failure of hair regrowth in doxycycline-treated mice
• failure of regression at P20 in doxycycline-treated mice and remained in an abnormal growth phase
• following hair plucking, doxycycline-treated mice fail to sustain hair growth unlike control mice
• after P14 in doxycycline-treated mice
• external hair becomes wavy between P12 and P14 in doxycycline-treated mice
• in doxycycline-treated mice likely due to matrix cell apoptosis
• at P17 in doxycycline-treated mice after degradation begins
• fewer differentiation cell in doxycycline-treated mice following plucking-induced anagen initiation
• with extrusion of abnormally keratinized cellular material in doxycycline-treated mice
• in doxycycline-treated mice following plucking-induced anagen initiation
• failure of catagen in doxycycline-treated mice
• failure of regression at P20 in doxycycline-treated mice
• by P20, doxycycline-treated mice exhibit thickened interfollicular epidermis compared with control mice
• mice treated with doxycycline exhibit a temporary phenotype of dry scaly skin that is resolved in an anterior-posterior direction
• mice treated with doxycycline exhibit a temporary phenotype of dry scaly skin that is resolved in an anterior-posterior direction

cellular
• doxycycline-treated mice exhibit matrix cell apoptosis with DNA damage response unlike in control mice

growth/size/body
• in doxycycline-treated mice




Genotype
MGI:5431583
cn3
Allelic
Composition
Dicer1tm1Smr/Dicer1tm1Smr
Tg(KRT5-rtTA)1Glk/0
Tg(tetO-cre)1Jaw/0
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dicer1tm1Smr mutation (1 available); any Dicer1 mutation (52 available)
Tg(KRT5-rtTA)1Glk mutation (0 available)
Tg(tetO-cre)1Jaw mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
N
• doxycycline-treated mice retain hair follicle stem cells in early telogen and anagen
• hair phenotype in doxycycline-treated mice appears more rapidly than in Droshatm1Litt/Droshatm1Litt Tg(KRT5-rtTA)1Glk Tg(tetO-cre)1Jaw mice
• failure of hair regrowth in doxycycline-treated mice
• failure of regression at P20 in doxycycline-treated mice and remained in an abnormal growth phase
• following hair plucking, doxycycline-treated mice fail to sustain hair growth unlike control mice
• after P14 in doxycycline-treated mice
• external hair becomes wavy between P12 and P14 in doxycycline-treated mice
• in doxycycline-treated mice likely due to matrix cell apoptosis
• at P17 in doxycycline-treated mice after degradation begins
• fewer differentiation cell in doxycycline-treated mice following plucking-induced anagen initiation
• at P59 doxycycline-treated mice exhibit loss of bulge stem cells unlike in control mice
• however, bulge stem cells are present at P20 and P22
• with extrusion of abnormally keratinized cellular material in doxycycline-treated mice
• in doxycycline-treated mice following plucking-induced anagen initiation
• failure of catagen in doxycycline-treated mice
• failure of regression at P20 in doxycycline-treated mice
• by P20, doxycycline-treated mice exhibit thickened interfollicular epidermis compared with control mice
• mice treated with doxycycline exhibit a temporary phenotype of dry scaly skin that is resolved in an anterior-posterior direction
• mice treated with doxycycline exhibit a temporary phenotype of dry scaly skin that is resolved in an anterior-posterior direction

cellular
• doxycycline-treated mice exhibit matrix cell apoptosis with DNA damage response unlike in control mice

growth/size/body
• in doxycycline-treated mice




Genotype
MGI:5317912
cx4
Allelic
Composition
Tg(KRT5-rtTA)1Glk/0
Tg(tetO/CMV-Tslp)#Sfz/0
Genetic
Background
C.Cg-Tg(KRT5-rtTA)1Glk Tg(tetO/CMV-Tslp)#Sfz
Find Mice Using the International Mouse Strain Resource (IMSR)
No mouse lines available in IMSR.
See publication links below for author information.
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• dox treated mutants develop autoimmune hemolytic anemia
• mature follicular B cells in doxycycline (dox) treated mutants display features of polyclonal activation, including down-regulation of CD21/CD35 expression, elevated CD23 and MHC class II expression, increased cell size and increased mitogenic responses
• following polyclonal stimulation in vitro, primary B cells from dox treated mutants exhibit higher levels of [3H] thymidine incorporation, indicating increased proliferation potential
• following anti-IgM and LPS stimulation, primary B cells from dox treated mutants, exhibit higher levels of BrdU incorporation, indicating increased proliferation potential
• dox treated mutants exhibit an increase in serum IL-4 levels
• following dox treatment, mutants show the presence of anti-RBC-specific autoantibodies

hematopoietic system
• dox treated mutants develop autoimmune hemolytic anemia
• following dox treatment, mutants show a decrease in hematocrit corresponding with the presence of anti-RBC-specific autoantibodies, consistent with onset of hemolytic anemia
• mature follicular B cells in doxycycline (dox) treated mutants display features of polyclonal activation, including down-regulation of CD21/CD35 expression, elevated CD23 and MHC class II expression, increased cell size and increased mitogenic responses
• following polyclonal stimulation in vitro, primary B cells from dox treated mutants exhibit higher levels of [3H] thymidine incorporation, indicating increased proliferation potential
• following anti-IgM and LPS stimulation, primary B cells from dox treated mutants, exhibit higher levels of BrdU incorporation, indicating increased proliferation potential

homeostasis/metabolism
• dox treated mutants exhibit an increase in serum IL-4 levels

Mouse Models of Human Disease
OMIM ID Ref(s)
Anemia, Autoimmune Hemolytic 205700 J:182756




Genotype
MGI:5317870
cx5
Allelic
Composition
Tcrbtm1Mom/Tcrbtm1Mom
Tg(KRT5-rtTA)1Glk/0
Tg(tetO/CMV-Tslp)#Sfz/0
Genetic
Background
involves: 129P2/OlaHsd * C3H * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tcrbtm1Mom mutation (12 available); any Tcrb mutation (77 available)
Tg(KRT5-rtTA)1Glk mutation (0 available)
Tg(tetO/CMV-Tslp)#Sfz mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
• mutants treated with dox for 3 weeks exhibit dermal infiltration mostly of mast cells and eosinophils
• mutants treated with doxycycline (dox) for 3 weeks exhibit dermal infiltration mostly of mast cells and eosinophils
• mutants treated with dox for 3 weeks exhibit epidermal thickening

immune system
• dox treated mice exhibit little or no serum IgE
• mutants treated with dox for 3 weeks exhibit dermal infiltration mostly of mast cells and eosinophils

hematopoietic system
• dox treated mice exhibit little or no serum IgE




Genotype
MGI:5317865
cx6
Allelic
Composition
Tg(KRT5-rtTA)1Glk/0
Tg(tetO/CMV-Tslp)#Sfz/0
Genetic
Background
involves: C3H * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
No mouse lines available in IMSR.
See publication links below for author information.
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
• by 5 weeks of doxycycline (dox) treatment, lesional skin shows characteristic changes of eczematous inflammation including spongiosis
• mutants treated with doxycycline (dox) to induce expression of Tslp develop skin disease beginning at about 2-3 weeks of dox treatment
• dox treated mutants exhibit dermal infiltrates containing lymphocytes, macrophages, mast cells, and eosinophils
• however, inflammation is not seen in the small intestine or colon
• by 5 weeks of dox treatment, lesional skin shows characteristic changes of eczematous inflammation including hyperkeratosis
• by 5 weeks of dox treatment, lesional skin shows characteristic changes of eczematous inflammation including acanthosis
• majority of dox treated mice exhibit a mild xerosis
• seen in dox treated mutants
• dox treated mutants exhibit skin lesions consisting of mild erythema at 2 weeks of dox treatment with progression to eczematous-like changes, including erythema, crusting, and erosions, by 3-4 weeks of dox treatment
• skin lesions are most common on the snout, postauricular region, nape of the neck and upper back
• less commonly, lesions are seen on the anterior neck and hind legs

immune system
• dox treated mutants exhibit an increase in the frequency of and absolute numbers of IL-4 producing Th2 CD4+ T cells in both the spleens and lymph nodes
• dox treated mutants exhibit splenomegaly
• in dox treated mutants
• in dox treated mutants
• in dox treated mutants
• dox treated mutants exhibit an increase in Th2 cytokines in effected skin
• dox treated mutants exhibit a 14-fold increase in IL-4 producing cells in the skin-draining lymph nodes and an 18-fold increase in the intestinal mesenteric lymph nodes
• dox treated mutants exhibit lymphadenopathy
• a few dox treated mice exhibit conjunctivitis
• mutants treated with doxycycline (dox) to induce expression of Tslp develop skin disease beginning at about 2-3 weeks of dox treatment
• dox treated mutants exhibit dermal infiltrates containing lymphocytes, macrophages, mast cells, and eosinophils
• however, inflammation is not seen in the small intestine or colon

hematopoietic system
• dox treated mutants exhibit an increase in the frequency of and absolute numbers of IL-4 producing Th2 CD4+ T cells in both the spleens and lymph nodes
• dox treated mutants exhibit splenomegaly
• in dox treated mutants
• in dox treated mutants
• in dox treated mutants

homeostasis/metabolism
• by 5 weeks of doxycycline (dox) treatment, lesional skin shows characteristic changes of eczematous inflammation including spongiosis
• dox treated mutants exhibit an increase in Th2 cytokines in effected skin

vision/eye
• a few dox treated mice exhibit conjunctivitis

Mouse Models of Human Disease
OMIM ID Ref(s)
Dermatitis, Atopic 603165 J:100506




Genotype
MGI:5503059
cx7
Allelic
Composition
Tg(KRT5-rtTA)1Glk/0
Tg(tetO-Tfrc/EGFP/Ova)#Sfz/0
Tg(tetO/CMV-Tslp)#Sfz/0
Genetic
Background
involves: C3H * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
No mouse lines available in IMSR.
See publication links below for author information.
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• of ovalbumin-specific CD4 T cells in doxycycline-treated mice unlike when cells are transferred into control mice
• airway inflammation in doxycycline-treated mice treated intranasally with ovalbumin
• eczematous inflammation in the skin of doxycycline- and anti-mTSLP antibody-treated mice

integument
• eczematous inflammation in the skin of doxycycline- and anti-mTSLP antibody-treated mice

respiratory system
• airway inflammation in doxycycline-treated mice treated intranasally with ovalbumin

hematopoietic system
• of ovalbumin-specific CD4 T cells in doxycycline-treated mice unlike when cells are transferred into control mice




Genotype
MGI:3815535
cx8
Allelic
Composition
Tg(KRT5-rtTA)1Glk/0
Tg(tetO-TGFB1*C223S*C225S)1Glk/0
Genetic
Background
involves: FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
No mouse lines available in IMSR.
See publication links below for author information.
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• double-transgenic mice with normal morphology are born at expected ratios when no doxycycline treatment is given to the dam

immune system
• epidermis of weaning-aged mice dosed with doxycycline displays a variable neutrophilic infiltrate characterized by microabcesses within and above cornified layers
• weaning-aged mice dosed with doxycycline develop dermatitis on scalp and shoulders, as well as ventral surface, within 3-4 weeks; dermatitis extends caudally with time

cellular
• treatment with doxycycline induces keratinocyte apoptosis
• cell proliferation in hyperplastic dermis of doxycycline-treated animals is elevated
• when adult mice undergo depilation and receive doxycycline treatment, cell proliferation is significantly reduced compared to mice which receive no doxycycline or single-transgenic controls

integument
• treatment with doxycycline induces keratinocyte apoptosis
• epidermis of weaning-aged mice dosed with doxycycline displays a variable neutrophilic infiltrate characterized by microabcesses within and above cornified layers
• weaning-aged mice dosed with doxycycline develop dermatitis on scalp and shoulders, as well as ventral surface, within 3-4 weeks; dermatitis extends caudally with time
• weaning-aged mice dosed with doxycycline display progressive hair loss within 3-4 weeks
• in weaning-aged mice dosed with doxycycline, many hair follicles appear hyperplastic with abnormal morphologies
• in animals treated with doxycycline, nearly all hair follicles have proliferating cells in the outer root sheath particularly in the infundibular region
• hair follicle density is significantly reduced in weaning-aged mice dosed with doxycycline
• treatment of animals with doxycycline causes keratinocytes to undergo growth arrest
• increased cellularity is observed in weaning-aged mice dosed with doxycycline
• significant thickening is observed in weaning-aged mice dosed with doxycycline
• weaning-aged mice dosed with doxycycline develop hyperkeratosis within 3-4 weeks
• epidermis of affected mice (weanlings treated with doxycycline) becomes acanthotic
• epidermis of affected mice (weanlings treated with doxycycline) exhibits hyperplasia




Genotype
MGI:5503058
cx9
Allelic
Composition
Tg(KRT5-rtTA)1Glk/0
Tg(tetO-Tfrc/EGFP/Ova)#Sfz/0
Genetic
Background
involves: FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
No mouse lines available in IMSR.
See publication links below for author information.
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
N
• doxycycline- and anti-mTSLP antibody-treated mice do not exhibit eczematous inflammation

integument
N
• doxycycline- and anti-mTSLP antibody-treated mice do not exhibit eczematous inflammation





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Tumor Biology (MTB), Gene Ontology (GO), MouseCyc
Citing These Resources
Funding Information
Warranty Disclaimer & Copyright Notice
Send questions and comments to User Support.
last database update
11/22/2016
MGI 6.06
The Jackson Laboratory