JAX
Mouse Strain Datasheet - 008180
129S/Sv-Krastm4Tyj/J
This strain carries a point mutation (G12D) in the Kras (v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog) gene whose expression is blocked by the presence of a loxP-flanked stop codon. Homozygotes die in utero. Cre-mediated recombination can excise the stop codon and permit the oncogenic protein to be expressed. Intranasal infection with an adenovirus encoding Cre results in a very high frequency of lung tumors and permits controlled timing of tumor initiation and tumor multiplicity. This strain may be useful in studies of cancer and development.
Donating Investigator
Dr. Tyler Jacks, Massachusetts Institute of Technology
Genetic overview
| Genetic Background | Generation |
|---|---|
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Krastm4Tyj
| Allele Type | Gene Symbol | Gene Name |
|---|---|---|
| Targeted (Conditional ready (e.g. floxed), No functional change) | Kras | Kirsten rat sarcoma viral oncogene homolog |
Research Applications
- Cancer Research
- Developmental Biology Research
- Research Tools
Detailed Description
This strain carries a point mutation (G12D) whose expression is blocked by the presence of a loxP-flanked stop codon. Homozygotes die in utero. Cre-mediated recombination can excise the stop codon and permit the oncogenic protein to be expressed. Intranasal infection with an adenovirus encoding Cre results in a very high frequency of lung tumors and permits controlled timing of tumor initiation and tumor multiplicity. This strain may be useful in studies of cancer and development.
When bred to a strain expressing Cre recombinase under the control of a tetracycline-responsive promoter element and a strain expressing a tetracycline-controlled activator protein in lung epithelial cells (see Stock No. 006234 and 006235 respectively), this mutant mouse strain may be useful in studies of lung development.
When bred to a strain expressing Cre recombinase in the male germ line (see Stock No. 003328, 007252 for example), this mutant mouse strain may be useful in studies of embryonic development.
When bred to a strain expressing interferon inducible Cre recombinase (see Stock No. 003556, 005673 for example), this mutant mouse strain may be useful in studies of Ras and myeloproliferative disease.
When bred to a strain expressing Cre recombinase in mammary gland, skin, and other secretory glands (see Stock No. 003553 for example), this mutant mouse strain may be useful in studies of epithelial hyperplasias.
When bred to a strain expressing Cre recombinase in epiblast derived tissues (see Stock No. 003755 for example), this mutant mouse strain may be useful in studies of Ras and embryonic development.
When bred to a strain expressing tamoxifen inducible Cre recombinase (see Stock No. 008463 for example), this mutant mouse strain may be useful in studies of tumorigenesis in the colon.
When bred to a strain expressing tamoxifen-inducible Cre recombinase in melanocytes (see Stock No. 012328 for example), this mutant mouse strain may be useful in studies of melanomagenesis.
When bred to a strain expressing Cre recombinase in astrocytes (see Stock No. 012887 for example), this mutant mouse strain may be useful in studies of neurofibroma development.
Development
A targeting vector was designed to place a G12D point mutation in exon 1 of the gene and a loxP-flanked STOP element upstream of the mutation. The STOP element incorporates a PGK-puromycin selection cassette at the 5' end in an opposite directional orientation. An adenoviral strong splice acceptor, typically used in gene trap vectors, is fused upstream of the his3 stuffer fragment to prevent splicing around the stopper (in the case that transcription isn't completely silenced). A mutant splice donor site is on the 3' end and a tetrameric tandem array of SV40 PolyA. The stopper was designed to fit into genomic Sal1 or Xho1 sites. The stop cassette prevents the expression of mutant Kras until it is removed by Cre mediated recombination of the loxP sites, thus allowing expression of oncogenic Kras. The construct was electroporated into 129S4/SvJae-derived J1 embryonic stem (ES) cells. This strain was crossed to 129S4/SvJae for more than 10 generations by the donating laboratory which verified correct orientation by Southern assays involving 5' and 3' external and internal probes.
Selected References
- Jackson EL; Willis N; Mercer K; Bronson RT; Crowley D; Montoya R; Jacks T; Tuveson DA. 2001. Analysis of lung tumor initiation and progression using conditional expression of oncogenic K-ras. Genes Dev 15(24):3243-8. PubMed: 11751630MGI: J:73445
Krastm4Tyj
Allele Symbol: Krastm4Tyj
| Allele Name | targeted mutation 4, Tyler Jacks |
|---|---|
| Allele Type | Targeted (Conditional ready (e.g. floxed), No functional change) |
| Allele Synonym(s) | K-Ras(G12D)fl; K-RasL; K-RasG12D; K-rasLSL; KR; Kras2tm4Tyj; Kras2tm14Tyj; KrasG12D; KrasLSL-G12D; KrasLox; LSL-K-ras G12D; LSL-K-rasG12D; LSL-Kras G12D; LSL-KrasG12D; LSL-KrasG12D; Lox-Stop-Lox-KrasG12D; caKRas |
| Gene Symbol and Name | Kras, Kirsten rat sarcoma viral oncogene homolog |
| Gene Synonym(s) | AI929937; C-K-RAS; CFC2; K-RAS2A; K-RAS2B; K-RAS4A; K-RAS4B; K-ras; KI-RAS; KRAS1; KRAS2; Ki-ras; Kirsten rat sarcoma oncogene 2, expressed; Kras-2; Kras-2; Kras2; Kras2; NS; NS3; RALD; RASK2; c-Ki-ras; c-Ki-ras2; expressed sequence AI929937; p21 |
| Strain of Origin | 129S4/SvJae |
| Chromosome | 6 |
| Molecular Note | By homologous recombination in ES cells, the Kras2 locus was targeted with a cassette containing an oncogenic form of the KRAS2 protein in which the glycine at position 12 had been substituted with a an aspartic acid. A loxP flanked stop codon was included upstream of the inserted Kras2 sequence, such that the mutant transcript would be expressed only after cre-mediated recombination. |
| Mutations Made By | Dr. Tyler Jacks, Massachusetts Institute of Technology |
Disease Terms
Research Areas By Genotype
This mouse can be used to support research in many areas including:
- Cancer Research
- Increased Tumor Incidence
- Other Tissues/Organs
- Other Tissues/Organs: lung
- Increased Tumor Incidence
- Developmental Biology Research
- Embryonic Lethality (Homozygous)
- Research Tools
- Cre-lox System
- loxP-flanked Sequences
- Cre-lox System
Mammalian Phenotype Terms by Genotype
Genotype: Krastm4Tyj/Kras+
either: (involves: 129S4/SvJae) or (involves: 129S4/SvJae * C3H/HeJ)
endocrine/exocrine gland phenotype
- abnormal ovary morphology
- after ovarian intrabursal injection of an adenovirus expressing Cre, mutants develop benign ovarian endometriosis-like lesions, however no invasive ovarian tumors are seen up to 10 months following adenoviral injection (MGI Ref ID J:96296)
growth/size/body region phenotype
- abnormal peritoneum morphology
reproductive system phenotype
- abnormal ovary morphology
- after ovarian intrabursal injection of an adenovirus expressing Cre, mutants develop benign ovarian endometriosis-like lesions, however no invasive ovarian tumors are seen up to 10 months following adenoviral injection (MGI Ref ID J:96296)
The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain
Genotype: Krastm4Tyj/Kras+
involves: 129S4/SvJae
neoplasm
- increased lung adenocarcinoma incidence
- increased lung adenoma incidence
- mice develop lung adenomas with a few adenocarcinomas following intratracheal administration of an adenovirus expressing Cre (Ad-Cre) (MGI Ref ID J:207982)
- treatment with MLN4924, a small molecular inhibitor of NAE, beginning at 13 weeks after Ad-Cre administration reduces tumor burden, with a reduction in both number of hyperplastic areas and adenomas and size of the tumors (MGI Ref ID J:207982)
- presence of atypical adenomatous hyperplasia after Cre-adenovirus treatment (MGI Ref ID J:158937)
- increased lung tumor incidence
- 20% and 100% of mice develop lung lesions at 6 weeks and 20 weeks, respectively, post intranasal adenoviral cre administration (MGI Ref ID J:216266)
- treatment with adenoviral Cre to induce oncogenic Kras expression results in lung tumor development, but causes a lower tumor burden and decreased overall tumor area compared to induced mutants on a Spry2-null background (MGI Ref ID J:119477)
- cre adenovirus-treated mice develop fewer tumors than in Krastm4Tyj/Kras+ Rb1tm3Tyj/Rb1tm3Tyj mice (MGI Ref ID J:147590)
- cre adenovirus-treated mice develop lung adenocarcinomas, papillary adenomas and bronchiolar hyperplasia and dysplasia (MGI Ref ID J:147590)
- large tumors easily visible on the surface of the lungs at eight weeks after Cre-adenovirus treatment (MGI Ref ID J:158937)
- mice treated with adenovirus cre develop lung lesions in 4 to 6 months (MGI Ref ID J:147590)
- abnormal tumor morphology
- tumors from cre adenovirus-treated mice exhibit increased cell proliferation compared to in tumors from Krastm4Tyj/Kras+ Rbl2tm2Tyj/Rbl2tm2Tyj mice (MGI Ref ID J:147590)
- decreased tumor growth/size
- cre adenovirus-treated mice develop smaller tumors than in cre adenovirus-treated Krastm4Tyj/Kras+ Rbl2tm2Tyj/Rbl2tm2Tyj mice (MGI Ref ID J:147590)
- increased lung carcinoma incidence
- the most common lesion is adenocarcinoma after Cre-adenovirus treatment (MGI Ref ID J:158937)
mortality/aging
- premature death
- median life span of cre adenovirus-treated mice is 32 weeks (MGI Ref ID J:147590)
respiratory system phenotype
- abnormal bronchiole morphology
- cre adenovirus-treated mice develop bronchiolar hyperplasia and dysplasia unlike wild-type mice (MGI Ref ID J:147590)
- bronchiolar epithelial hyperplasia
- in cre adenovirus-treated mice (MGI Ref ID J:147590)
- increased lung adenocarcinoma incidence
- increased lung adenoma incidence
- presence of atypical adenomatous hyperplasia after Cre-adenovirus treatment (MGI Ref ID J:158937)
- mice develop lung adenomas with a few adenocarcinomas following intratracheal administration of an adenovirus expressing Cre (Ad-Cre) (MGI Ref ID J:207982)
- treatment with MLN4924, a small molecular inhibitor of NAE, beginning at 13 weeks after Ad-Cre administration reduces tumor burden, with a reduction in both number of hyperplastic areas and adenomas and size of the tumors (MGI Ref ID J:207982)
- increased lung carcinoma incidence
- the most common lesion is adenocarcinoma after Cre-adenovirus treatment (MGI Ref ID J:158937)
- increased lung tumor incidence
- cre adenovirus-treated mice develop fewer tumors than in Krastm4Tyj/Kras+ Rb1tm3Tyj/Rb1tm3Tyj mice (MGI Ref ID J:147590)
- cre adenovirus-treated mice develop lung adenocarcinomas, papillary adenomas and bronchiolar hyperplasia and dysplasia (MGI Ref ID J:147590)
- large tumors easily visible on the surface of the lungs at eight weeks after Cre-adenovirus treatment (MGI Ref ID J:158937)
- mice treated with adenovirus cre develop lung lesions in 4 to 6 months (MGI Ref ID J:147590)
- 20% and 100% of mice develop lung lesions at 6 weeks and 20 weeks, respectively, post intranasal adenoviral cre administration (MGI Ref ID J:216266)
- treatment with adenoviral Cre to induce oncogenic Kras expression results in lung tumor development, but causes a lower tumor burden and decreased overall tumor area compared to induced mutants on a Spry2-null background (MGI Ref ID J:119477)
- lung epithelium hyperplasia
- presence of epithelial hyperplasia after Cre-adenovirus treatment (MGI Ref ID J:158937)
- thick pulmonary interalveolar septum
- in cre adenovirus-treated mice (MGI Ref ID J:147590)
immune system phenotype
- increased regulatory T cell number
- following injection of a cre adenovirus in the ovarian bursa, mice with endometriosis also exhibit an increase in spleen and regional lymph nodes T regulatory cells compared with un-injected Krastm4Tyj Tg(MUC1)79.24Gend mice (MGI Ref ID J:154046)
hematopoietic system phenotype
- increased regulatory T cell number
- following injection of a cre adenovirus in the ovarian bursa, mice with endometriosis also exhibit an increase in spleen and regional lymph nodes T regulatory cells compared with un-injected Krastm4Tyj Tg(MUC1)79.24Gend mice (MGI Ref ID J:154046)
reproductive system phenotype
- uterus adenomyosis
- following injection of a cre adenovirus in the ovarian bursa, mice develop ovarian lesions consisting of endometrial glandular epithelium unlike un-injected Krastm4Tyj micefollowing injection of a cre adenovirus in the ovarian bursa, mice develop ovarian lesions consisting of endometrial glandular epithelium unlike un-injected Krastm4Tyj miceop ovarian lesions consisting of endometrial glandular epithelium unlike un-injected Krastm4Tyj mice (MGI Ref ID J:154046)
Genotype: Krastm4Tyj/Kras+
involves: 129S4/SvJae * C57BL/6
respiratory system phenotype
- increased lung adenoma incidence
- lung adenocarcinomas cover 11% of lung area 9 weeks after administration of a Cre-recombinase expressing adenovirus (MGI Ref ID J:203686)
neoplasm
- increased lung adenoma incidence
- lung adenocarcinomas cover 11% of lung area 9 weeks after administration of a Cre-recombinase expressing adenovirus (MGI Ref ID J:203686)
Genotype: Krastm4Tyj/Kras+
involves: 129S4/SvJae * C57BL/6 * FVB/N
respiratory system phenotype
- increased lung adenocarcinoma incidence
- all tumors of ad-cre inoculated mice are adenocarincomas (MGI Ref ID J:124682)
- metastasis or local invasion is not seen in ad-cre inoculated mice (MGI Ref ID J:124682)
- mice inoculated with ad-cre by inhalation develop lung tumors with high multiplicity, long latency, and low aggressiveness (MGI Ref ID J:124682)
mortality/aging
- premature death
- mice inoculated with an adenovirus expressing cre recombinase (ad-cre) by inhalation have a median survival of 24 weeks after ad-cre inoculation (MGI Ref ID J:124682)
neoplasm
- increased lung adenocarcinoma incidence
- all tumors of ad-cre inoculated mice are adenocarincomas (MGI Ref ID J:124682)
- metastasis or local invasion is not seen in ad-cre inoculated mice (MGI Ref ID J:124682)
- mice inoculated with ad-cre by inhalation develop lung tumors with high multiplicity, long latency, and low aggressiveness (MGI Ref ID J:124682)
Genotype: Krastm4Tyj/Kras+
B6.129S4-Krastm4Tyj
respiratory system phenotype
- increased lung adenocarcinoma incidence
- mutants with an intranasal instillation of an adenovirus expressing Cre recombinase develop noninvasive adenoma and adenocarcinoma over a 6-10 week period, characterized by epithelial cell proliferation without destruction of alveolar walls or stromal reactionction (MGI Ref ID J:177379)
- increased lung adenoma incidence
- mutants with an intranasal instillation of an adenovirus expressing Cre recombinase develop noninvasive adenoma and adenocarcinoma over a 6-10 week period, characterized by epithelial cell proliferation without destruction of alveolar walls or stromal reactionction (MGI Ref ID J:177379)
mortality/aging
- premature death
- mutants with an intranasal instillation of an adenovirus expressing Cre recombinase have a median survival of 79 days (MGI Ref ID J:177379)
neoplasm
- increased lung adenocarcinoma incidence
- mutants with an intranasal instillation of an adenovirus expressing Cre recombinase develop noninvasive adenoma and adenocarcinoma over a 6-10 week period, characterized by epithelial cell proliferation without destruction of alveolar walls or stromal reactionction (MGI Ref ID J:177379)
- increased lung adenoma incidence
- mutants with an intranasal instillation of an adenovirus expressing Cre recombinase develop noninvasive adenoma and adenocarcinoma over a 6-10 week period, characterized by epithelial cell proliferation without destruction of alveolar walls or stromal reactionction (MGI Ref ID J:177379)
Genotype: Krastm4Tyj/Krastm4Tyj
B6.129S4-Krastm4Tyj
cellular phenotype
- increased cell proliferation
- primary mouse embryonic fibroblast treated with adenoviral-cre exhibit enhanced growth rate compared with wild-type cells (MGI Ref ID J:187371)
The following phenotype relates to a compound genotype created using this strain
Genotype: Krastm4Tyj/Kras+ Gt(ROSA)26Sortm1(cre/ERT2)Tyj/Gt(ROSA)26Sor+
involves: 129S4/SvJae
digestive/alimentary phenotype
- abnormal colon goblet cell morphology
- large, prominent goblet cells develop in the colon in adult mice (MGI Ref ID J:132357)
- abnormal intestinal epithelium morphology
- adult mice develop widespread hyperplasia throughout the colonic epithelium (MGI Ref ID J:132357)
- abnormal large intestine crypts of Lieberkuhn morphology
- hyperplasia is typified by lengthening of the crypts in adult mice (MGI Ref ID J:132357)
endocrine/exocrine gland phenotype
- abnormal colon goblet cell morphology
- large, prominent goblet cells develop in the colon in adult mice (MGI Ref ID J:132357)
- abnormal large intestine crypts of Lieberkuhn morphology
- hyperplasia is typified by lengthening of the crypts in adult mice (MGI Ref ID J:132357)
Genotype: Krastm4Tyj/Kras+ Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S4/SvJae
mortality/aging
- postnatal lethality, complete penetrance
- the maximum survival is 24 days (MGI Ref ID J:158937)
respiratory system phenotype
- increased lung tumor incidence
- (MGI Ref ID J:158937)
- increased lung weight
- lung weight is 10-fold higher than that in control mice at 3 weeks old (MGI Ref ID J:158937)
neoplasm
- increased lung tumor incidence
- (MGI Ref ID J:158937)
Genotype: Krastm4Tyj/Kras+ Tg(Alb-cre)21Mgn/0
involves: 129S4/SvJae * C57BL/6 * DBA
liver/biliary system phenotype
- increased cholangiocarcinoma incidence
- mutants develop invasive intrahepatic cholangiocarcinoma with low penetrance (1 of 8 mutants) and long latency (at 36 weeks of age) (MGI Ref ID J:184949)
neoplasm
- increased cholangiocarcinoma incidence
- mutants develop invasive intrahepatic cholangiocarcinoma with low penetrance (1 of 8 mutants) and long latency (at 36 weeks of age) (MGI Ref ID J:184949)
Genotype: Krastm4Tyj/Kras+ Tg(Fabp1-cre)1Jig/0
involves: 129S4/SvJae * FVB/N
digestive/alimentary phenotype
Genotype: Krastm4Tyj/Kras+ Tg(Gfap-cre)77.6Mvs/0
involves: 129 * BALB/c * C57BL/6NHsd
neoplasm
- neoplasm
- mutants do not develop tumors (MGI Ref ID J:154673)
Genotype: Krastm4Tyj/Kras+ Tg(IVL-cre/ERT2)1Blpn/0
involves: 129S4/SvJae * C57BL/6
neoplasm
- increased facial tumor incidence
- 2-4 months following tamoxifen treatment, tumors develop in the face in 40% of treated mutants (MGI Ref ID J:172048)
- increased lip tumor incidence
- 100% of animals develop lip tumors 2-4 months after tamoxifen treatment (MGI Ref ID J:172048)
- increased skin papilloma incidence
- increased skin tumor incidence
- 2-4 months following RU486 treatment, tumors develop in the back skin in 80% of treated mice (MGI Ref ID J:172048)
craniofacial phenotype
- increased facial tumor incidence
- 2-4 months following tamoxifen treatment, tumors develop in the face in 40% of treated mutants (MGI Ref ID J:172048)
- increased lip tumor incidence
- 100% of animals develop lip tumors 2-4 months after tamoxifen treatment (MGI Ref ID J:172048)
integument phenotype
- epidermal hyperplasia
- hyperplasia of the interfollicular epidermis in TAM treated mice (MGI Ref ID J:172048)
- increased skin papilloma incidence
- increased skin tumor incidence
- 2-4 months following RU486 treatment, tumors develop in the back skin in 80% of treated mice (MGI Ref ID J:172048)
- thick epidermis
- after tamoxifen treatment, hyperthickening of the interfollicular epidermis (IFE) is observed, indicating that hyperproliferation of IFE cells and hyperplasia of the IFE results from Kras LSL-G12D activation (MGI Ref ID J:172048)
growth/size/body region phenotype
- increased facial tumor incidence
- 2-4 months following tamoxifen treatment, tumors develop in the face in 40% of treated mutants (MGI Ref ID J:172048)
- increased lip tumor incidence
- 100% of animals develop lip tumors 2-4 months after tamoxifen treatment (MGI Ref ID J:172048)
Genotype: Krastm4Tyj/Kras+ Tg(KRT14-cre/ERT)20Efu/0
involves: 129S4/SvJae * C57BL/6 * CD-1 * FVB/N
digestive/alimentary phenotype
- increased mouth tumor incidence
- tamoxifen treated mice develop oral tumors (MGI Ref ID J:210533)
neoplasm
- increased mouth tumor incidence
- tamoxifen treated mice develop oral tumors (MGI Ref ID J:210533)
Genotype: Krastm4Tyj/Kras+ Tg(Krt1-15-cre/PGR)22Cot/0
involves: 129S4/SvJae * C57BL/6J * SJL/J
craniofacial phenotype
- increased facial tumor incidence
- 2-4 months following RU486 treatment, tumors develop in the face in 35% of treated mutants (MGI Ref ID J:172048)
- increased lip tumor incidence
- 2-4 months following RU486 treatment, lip tumors develop in 57% of treated mice (MGI Ref ID J:172048)
growth/size/body region phenotype
- increased facial tumor incidence
- 2-4 months following RU486 treatment, tumors develop in the face in 35% of treated mutants (MGI Ref ID J:172048)
- increased lip tumor incidence
- 2-4 months following RU486 treatment, lip tumors develop in 57% of treated mice (MGI Ref ID J:172048)
neoplasm
- increased facial tumor incidence
- 2-4 months following RU486 treatment, tumors develop in the face in 35% of treated mutants (MGI Ref ID J:172048)
- increased lip tumor incidence
- 2-4 months following RU486 treatment, lip tumors develop in 57% of treated mice (MGI Ref ID J:172048)
- increased skin papilloma incidence
- increased skin tumor incidence
- 2-4 months following RU486 treatment, tumors develop in the back skin in 14% of treated mice (MGI Ref ID J:172048)
integument phenotype
- increased skin papilloma incidence
- increased skin tumor incidence
- 2-4 months following RU486 treatment, tumors develop in the back skin in 14% of treated mice (MGI Ref ID J:172048)
Genotype: Krastm4Tyj/Kras+ Tg(Krt1-15-cre/PGR)22Cot/0
involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL/J
neoplasm
- increased papilloma incidence
- mice develop benign papillomas without progressing to malignancy following topical application of RU486 to the back of skin at 3 weeks of age for 5 days (MGI Ref ID J:203922)
Genotype: Krastm4Tyj/Kras+ Tg(MMTV-cre)4Mam/0
involves: 129S4/SvJae * FVB
endocrine/exocrine gland phenotype
- submandibular gland hyperplasia
- submandibular gland hyperplasia is seen in mutant mice (MGI Ref ID J:89333)
digestive/alimentary phenotype
- submandibular gland hyperplasia
- submandibular gland hyperplasia is seen in mutant mice (MGI Ref ID J:89333)
Genotype: Krastm4Tyj/Kras+ Tg(Mx1-cre)1Cgn/0
involves: 129S4/SvJae * C57BL/6 * CBA
mortality/aging
- premature death
- mice survive for a median of 84 days after pIpC injection (MGI Ref ID J:87429)
hematopoietic system phenotype
- abnormal erythropoiesis
- bone marrow from pIpC treated mice forms abnormally large BFU-E colonies characterized by both erythropoietin-independent growth and hypersensitivity to erythropoietin (MGI Ref ID J:115071)
- mice treated with pIpC show large numbers of proliferating splenic Ter199+ cells, indicating that erythropoiesis is ineffective (MGI Ref ID J:87429)
- pIpC treated mice show normal numbers of early erythroid cells in the bone marrow but a paucity of all the more mature TER119 hi populations, indicating an inefficient transition from TER119- to TER119 hi stages of erythropoiesis (MGI Ref ID J:115071)
- spleen of pIpC treated mice contains increase of immature CD71 hi TER119-/lo cells and large numbers of TER119 hi erythroblasts (MGI Ref ID J:115071)
- the erythroid progenitor compartment is massively expanded in the spleen of pIpC treated mice (MGI Ref ID J:115071)
- abnormal myelopoiesis
- CFU-GM shows an increased proliferative response without added cytokines (9-fold) or to GM-CSF (19-fold increase) or IL-3 (37-fold increase) (MGI Ref ID J:87429)
- bone marrow mononuclear cells from pIpC treated mice form significant numbers of colony-forming unit granulocyte-macrophage (CFU-GM) colonies in the absence of exogenous cytokines while wild-type cells do not (MGI Ref ID J:87429)
- pIpC injected mice develop a myeloproliferative disease with excess monocytes (MGI Ref ID J:87429)
- anemia
- anisopoikilocytosis
- in pIpC treated mice (MGI Ref ID J:115071)
- decreased mean corpuscular hemoglobin
- in pIpC treated mice (MGI Ref ID J:115071)
- enlarged spleen
- increased leukocyte cell number
- pups injected with pIpC at 21 days of age develop progressive leukocytosis that is evident 3 weeks after pIpC injection (MGI Ref ID J:87429)
- increased monocyte cell number
- mice show an expanded population of Mac-1+, Gr-1 lo cells, indicating an expansion of immature monocytic cells (MGI Ref ID J:87429)
- increased splenocyte proliferation
- increase in the number of proliferating splenocytes in pIpC treated mice; most of these proliferating cells are Mac1+/Gr1 lo or Ter119+ (MGI Ref ID J:87429)
- myeloid hyperplasia
- mice show abundant myeloid cells at various stages of differentiation after pIpC injection (MGI Ref ID J:87429)
- polychromatophilia
- in pIpC treated mice (MGI Ref ID J:115071)
- reticulocytosis
- in pIpC treated mice (MGI Ref ID J:115071)
immune system phenotype
- abnormal myelopoiesis
- CFU-GM shows an increased proliferative response without added cytokines (9-fold) or to GM-CSF (19-fold increase) or IL-3 (37-fold increase) (MGI Ref ID J:87429)
- bone marrow mononuclear cells from pIpC treated mice form significant numbers of colony-forming unit granulocyte-macrophage (CFU-GM) colonies in the absence of exogenous cytokines while wild-type cells do not (MGI Ref ID J:87429)
- pIpC injected mice develop a myeloproliferative disease with excess monocytes (MGI Ref ID J:87429)
- enlarged spleen
- increased leukocyte cell number
- pups injected with pIpC at 21 days of age develop progressive leukocytosis that is evident 3 weeks after pIpC injection (MGI Ref ID J:87429)
- increased monocyte cell number
- mice show an expanded population of Mac-1+, Gr-1 lo cells, indicating an expansion of immature monocytic cells (MGI Ref ID J:87429)
- increased splenocyte proliferation
- increase in the number of proliferating splenocytes in pIpC treated mice; most of these proliferating cells are Mac1+/Gr1 lo or Ter119+ (MGI Ref ID J:87429)
- myeloid hyperplasia
- mice show abundant myeloid cells at various stages of differentiation after pIpC injection (MGI Ref ID J:87429)
liver/biliary system phenotype
- enlarged liver
- pIpC injected mice show moderate hepatomegaly with myeloid infiltration, particularly in periportal areas (MGI Ref ID J:87429)
cellular phenotype
- increased splenocyte proliferation
- increase in the number of proliferating splenocytes in pIpC treated mice; most of these proliferating cells are Mac1+/Gr1 lo or Ter119+ (MGI Ref ID J:87429)
homeostasis/metabolism phenotype
- increased circulating erythropoietin level
- serum erythropoietin levels are increased in proportion to anemia in pIpC treated mice (MGI Ref ID J:115071)
Genotype: Krastm4Tyj/Kras+ Tg(Mx1-cre)1Cgn/0
involves: 129S4/SvJae * BALB/c * C57BL/6 * CBA
digestive/alimentary phenotype
- increased esophageal papilloma incidence
- 8 of 22 mice injected with pIpC develop squamous papillomas involving the esophageal mucosa (MGI Ref ID J:88163)
- increased oral papilloma incidence
respiratory system phenotype
- increased lung adenoma incidence
endocrine/exocrine gland phenotype
- increased lymphoblastic lymphoma incidence
mortality/aging
- premature death
neoplasm
- increased esophageal papilloma incidence
- 8 of 22 mice injected with pIpC develop squamous papillomas involving the esophageal mucosa (MGI Ref ID J:88163)
- increased lung adenoma incidence
- increased lymphoblastic lymphoma incidence
- increased oral papilloma incidence
- increased papilloma incidence
- squamous papillomas (MGI Ref ID J:88163)
- increased skin papilloma incidence
growth/size/body region phenotype
- cachexia
- becoming emaciated (MGI Ref ID J:88163)
hematopoietic system phenotype
- abnormal definitive hematopoiesis
- develop lethal hematopoietic disease (MGI Ref ID J:88163)
- abnormal erythrocyte morphology
- (MGI Ref ID J:88163)
- abnormal myelopoiesis
- 4-7 week old mice injected with pIpC develop a myeloproliferative disorder (MGI Ref ID J:88163)
- all mice that are not treated with pIpC also develop a hematopoietic disease, however these mice exhibit expression of the mutant Kras, indicating that most likely endogenous IFN expression is sufficient to induce the cre transgene (MGI Ref ID J:88163)
- bone marrow cells from pIpC injected mice readily form colonies, predominately monocyte colony-forming units (M-CFUs) in a growth factor-independent manner unlike controls (MGI Ref ID J:88163)
- bone marrow of mice injected with pIpC shows myelomonocytic expansion (MGI Ref ID J:88163)
- anemia
- mice injected with pIpC become anemic (MGI Ref ID J:88163)
- decreased hematocrit
- mice injected with pIpC have a mean hematocrit of 27% compared with 45% in controls (MGI Ref ID J:88163)
- enlarged spleen
- mice injected with pIpC develop moderate to severe splenomegaly (MGI Ref ID J:88163)
- extramedullary hematopoiesis
- erythroid expansion was seen in red pulp of spleen in 5 of 16 cases (MGI Ref ID J:88163)
- expansion of red pulp in spleen by granulocyte/monocyte lineages in 11 out of 16 cases (MGI Ref ID J:88163)
- the liver shows perivascular and periportal infiltration by myeloid and erythroid cell populations (MGI Ref ID J:88163)
- increased granulocyte number
- leukocytosis in mice injected with pIpC is mainly due to an increase in granulocyte population (MGI Ref ID J:88163)
- increased leukocyte cell number
- leukocytosis, usually involving increases in granulocytes, in both pIpC and non-pIpC treated mice (MGI Ref ID J:88163)
- increased spleen red pulp amount
- mice injected with pIpC show expansion of the red pulp by varying degrees of granulocytic (MGI Ref ID J:88163)
- myeloid hyperplasia
immune system phenotype
- abnormal myelopoiesis
- 4-7 week old mice injected with pIpC develop a myeloproliferative disorder (MGI Ref ID J:88163)
- all mice that are not treated with pIpC also develop a hematopoietic disease, however these mice exhibit expression of the mutant Kras, indicating that most likely endogenous IFN expression is sufficient to induce the cre transgene (MGI Ref ID J:88163)
- bone marrow cells from pIpC injected mice readily form colonies, predominately monocyte colony-forming units (M-CFUs) in a growth factor-independent manner unlike controls (MGI Ref ID J:88163)
- bone marrow of mice injected with pIpC shows myelomonocytic expansion (MGI Ref ID J:88163)
- enlarged spleen
- mice injected with pIpC develop moderate to severe splenomegaly (MGI Ref ID J:88163)
- increased granulocyte number
- leukocytosis in mice injected with pIpC is mainly due to an increase in granulocyte population (MGI Ref ID J:88163)
- increased leukocyte cell number
- leukocytosis, usually involving increases in granulocytes, in both pIpC and non-pIpC treated mice (MGI Ref ID J:88163)
- increased spleen red pulp amount
- mice injected with pIpC show expansion of the red pulp by varying degrees of granulocytic (MGI Ref ID J:88163)
- lymphoid hyperplasia
- 6 of 17 mice injected with pIpC develop nodal lymphoid hyperplasia (MGI Ref ID J:88163)
- myeloid hyperplasia
liver/biliary system phenotype
- abnormal hepatobiliary system morphology
- perivascular and periportal infiltration in liver by myeloid and erythroid cells similar to what is seen in spleen (MGI Ref ID J:88163)
integument phenotype
- increased skin papilloma incidence
- ruffled hair
- ruffled fur (MGI Ref ID J:88163)
Genotype: Krastm4Tyj/Kras+ Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * C57BL/6 * FVB/N
neoplasm
- increased pancreatic intraepithelial neoplasia incidence
digestive/alimentary phenotype
- abnormal pancreatic duct morphology
- mice develop a varying number of ductal cell proliferation foci in the pancreas from 9 weeks after birth (MGI Ref ID J:214846)
endocrine/exocrine gland phenotype
- abnormal pancreatic duct morphology
- mice develop a varying number of ductal cell proliferation foci in the pancreas from 9 weeks after birth (MGI Ref ID J:214846)
Genotype: Krastm4Tyj/Kras+ Tg(Pdx1-cre)6Tuv/?
involves: 129S4/SvJae * FVB/N
neoplasm
- increased pancreatic ductal adenocarcinoma incidence
- by 7-10 months occasional animals with invasive and metastatic adenocarcinomas (MGI Ref ID J:87973)
- lesions eventually found in liver diaphragm and lungs (MGI Ref ID J:87973)
- number and extent of lesions increases with age (MGI Ref ID J:87973)
- transitions of epithelium from cuboid to columnar as early as 2 weeks (MGI Ref ID J:87973)
endocrine/exocrine gland phenotype
- enlarged pancreas
- (MGI Ref ID J:87973)
- increased pancreatic ductal adenocarcinoma incidence
- by 7-10 months occasional animals with invasive and metastatic adenocarcinomas (MGI Ref ID J:87973)
- lesions eventually found in liver diaphragm and lungs (MGI Ref ID J:87973)
- number and extent of lesions increases with age (MGI Ref ID J:87973)
- transitions of epithelium from cuboid to columnar as early as 2 weeks (MGI Ref ID J:87973)
Genotype: Krastm4Tyj/Kras+ Tg(Tyr-cre/ERT2)13Bos/0
involves: 129S4/SvJae * FVB
neoplasm
- increased melanoma incidence
- 1 in 14 tamoxifen treated mice develops melanoma with a median tumor latency greater than 52 weeks (MGI Ref ID J:164588)
pigmentation phenotype
- abnormal melanocyte morphology
- tamoxifen-treated mice exhibit melanocytic proliferation unlike wild-type mice (MGI Ref ID J:164588)
- hyperpigmentation
- tamoxifen-treated mice develop pigmented macules in the paws and tail unlike wild-type mice (MGI Ref ID J:164588)
Genotype: Krastm4Tyj/Krastm4Tyj Tg(SFTPC-rtTA)5Jaw/0 Tg(tetO-cre)1Jaw/0
involves: 129/Sv * C57BL/6
mortality/aging
- postnatal lethality, complete penetrance
- death in the early postnatal period (MGI Ref ID J:119477)
respiratory system phenotype
- abnormal branching involved in lung morphogenesis
- at E16.5, lungs show even more severe defects than in Kras:Meox2-cre embryos, with large epithelial-lined pouches in place of finely branched network of airways seen in wild-type (MGI Ref ID J:119477)
- branching defect persists through late gestation leading to early postnatal lethality (MGI Ref ID J:119477)
- with doxycycline treatment beginning at E6.5, a dramatic lung branching defect is observed (MGI Ref ID J:119477)
- abnormal bronchus epithelium morphology
- markers of ciliated and Clara cells in the bronchi are significantly reduced at E18.5 compared to controls, indicating block in differentiation of lung epithelium (MGI Ref ID J:119477)
- abnormal lung epithelium morphology
- branching defect originates in epithelium rather than mesenchyme (MGI Ref ID J:119477)
Genotype: Krastm4Tyj/Krastm4Tyj Tg(Tek-cre)12Flv/0
involves: 129S4/SvJae * C3H * C57BL/6
embryo phenotype
- embryo phenotype
- mutants show normal vascularization of the yolk sac and placental labyrinth (MGI Ref ID J:119477)
Genotype: Krastm4Tyj/Kras+ Meox2tm1(cre)Sor/Meox2+
involves: 129S4/SvJae * 129S4/SvJaeSor
mortality/aging
- embryonic lethality during organogenesis, incomplete penetrance
- embryos are recovered at a lower frequency (15% vs expected 25%) at E13.5 (MGI Ref ID J:119477)
- lethality throughout fetal growth and development, complete penetrance
- homozygous embryos die by E14.5 (MGI Ref ID J:119477)
embryo phenotype
- abnormal embryonic erythropoiesis
- fetal-derived hematopoietic progenitors form larger CFU-E (colony-forming unit-erythroid) and BFU-E (burst-forming unit-erythroid) colonies compared with controls (MGI Ref ID J:119477)
- embryo phenotype
- mutants show normal vascularization of the yolk sac and placental labyrinth (MGI Ref ID J:119477)
cardiovascular system phenotype
- abnormal atrioventricular valve morphology
- atrioventricular valve malformations (MGI Ref ID J:119477)
- abnormal cardiovascular system physiology
- heart defects lead to heart failure and death in embryos by ~E14.5 (MGI Ref ID J:119477)
- conotruncal ridge hyperplasia
- excess cushion tissue often leads to obstructed outflow tract (MGI Ref ID J:119477)
- double outlet right ventricle
- at E13.5, embryos frequently show double outlet right ventricle (MGI Ref ID J:119477)
- hemorrhage
- embryos appear normal at E12.5, but rapidly develop peripheral hemorrhages by E13.5, consistent with heart failure (MGI Ref ID J:119477)
- ventricular septal defect
- all embryonic hearts have prominent septal defects (MGI Ref ID J:119477)
hematopoietic system phenotype
- abnormal embryonic erythrocyte morphology
- red blood cells appear immature compared to wild-type and occasionally highly atypical, consisten with a block in erythroid differentiation (MGI Ref ID J:119477)
- abnormal embryonic erythropoiesis
- fetal-derived hematopoietic progenitors form larger CFU-E (colony-forming unit-erythroid) and BFU-E (burst-forming unit-erythroid) colonies compared with controls (MGI Ref ID J:119477)
respiratory system phenotype
- abnormal branching involved in lung morphogenesis
- abnormal bronchus morphology
- at E12.5, lungs exhibit large dilated bronchi; defect is more pronounced at E14.5 (MGI Ref ID J:119477)
- dilated respiratory conducting tubes
- at E12.5, lungs exhibit large dilated bronchi; defect is more pronounced at E14.5 (MGI Ref ID J:119477)
- impaired branching involved in bronchus morphogenesis
- impaired branching involved in terminal bronchiole morphogenesis
- at E14.5, mutants lungs display only a few terminal bronchioles (MGI Ref ID J:119477)
liver/biliary system phenotype
- increased hepatocyte apoptosis
- at E12.5 fetal livers show large areas of apoptosis (MGI Ref ID J:119477)
- liver hypoplasia
- at E12.5, fetal livers appear hypocellular (MGI Ref ID J:119477)
homeostasis/metabolism phenotype
- edema
- embryos appear normal at E12.5, but rapidly develop edema by E13.5, consistent with heart failure (MGI Ref ID J:119477)
integument phenotype
- pallor
- embryos appear normal at E12.5, but rapidly develop pallor by E13.5, consistent with heart failure (MGI Ref ID J:119477)
cellular phenotype
- increased hepatocyte apoptosis
- at E12.5 fetal livers show large areas of apoptosis (MGI Ref ID J:119477)
Genotype: Krastm4Tyj/Kras+ Shhtm2(cre/ERT2)Cjt/Shh+
involves: 129S4/SvJae * 129S6/SvEvTac
integument phenotype
- integument phenotype
- no epidermal defects or tumor formation are observed with tamoxifen treatment at day 28 (during period of up to 4 months after cre induction) when hair follicles are in full anlagen (MGI Ref ID J:172048)
References
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Additional - Krastm4Tyj related
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