Phenotypes associated with this allele

• Allele Symbol: Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}
• Allele Name: targeted mutation 14, Hongkui Zeng
• Allele ID: MGI:3809524
• Summary: 25 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
ht1	Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor^+	involves: 129S6/SvEvTac * C57BL/6NCr	MGI:4436847
cn2	Gt(ROSA)26Sor^tm1(GNAQ*)Cvrk/Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze Tg(Mitf-cre)7114Gsb/0	C3FeJ.Cg-Gt(ROSA)26Sor^tm1(GNAQ*)Cvrk/Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze Tg(Mitf-cre)7114Gsb/Cvrk	MGI:6792058
cn3	Wnt1^tm1.1Mze/Wnt1^tm1.1Mze Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor^+ En1^tm2(cre)Wrst/En1^+	involves: 129 * C57BL/6N	MGI:5495280
cn4	Celf2^tm1Yjin/Celf2^tm1Yjin Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor^+ Pvalb^tm1(cre)Arbr/Pvalb^+	involves: 129P2/OlaHsd * 129S6/SvEvTac * BALB/c * C57BL/6NCrl	MGI:6307011
cn5	Ednrb^tm1Nrd/Ednrb^tm1Nrd Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor^+ H2az2^Tg(Wnt1-cre)11Rth/H2az2^+	involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * C57BL/6 * CBA/J	MGI:5896991
cn6	Ednrb^tm1Nrd/Ednrb^tm1Nrd Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor^+ Tg(Tyr-cre/ERT2)13Bos/0	involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * C57BL/6J	MGI:6269398
cn7	Ets1^tm2Jml/Ets1^tm2Jml Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor^+ Pax3^tm1(cre)Joe/Pax3^+	involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * C57BL/6J * C57BL/6NCrl	MGI:7541421
cn8	Grin1^tm1c(EUCOMM)Wtsi/Grin1^tm2.1Stl Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor^+ Tg(Slc6a4-cre)ET127Gsat/0	involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * FVB/N * SJL	MGI:5485189
cn9	Kras^tm4Tyj/Kras^+ Tg(Cdh5-cre/ERT2)1Rha/0 Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6NCrl * FVB	MGI:7435431
cn10	Ctnna1^em1Xjz/Ctnna1^tm1Efu Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor^+ Tg(Pdgfb-icre/ERT2,-EGFP)1Frut/0	involves: 129S6/SvEvTac * 129X1/SvJ * C57BL/6 * C57BL/6J * C57BL/6NCrl * CBA	MGI:7467130
cn11	Ctnna1^tm1Efu/Ctnna1^tm1Efu Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor^+ Tg(Pdgfb-icre/ERT2,-EGFP)1Frut/0	involves: 129S6/SvEvTac * 129X1/SvJ * C57BL/6 * C57BL/6NCrl * CBA	MGI:7467113
cn12	Htr2c^tm2Jke/Y Tg(Pomc1-cre)16Lowl/0 Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor^+	involves: 129S6/SvEvTac * 129X1/SvJ * C57BL/6 * FVB/N	MGI:5569627
cn13	Nkx2-2^tm2.1Suss/Nkx2-2^tm2.1Suss Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor^+ Tg(Ins2-cre)23Herr/0	involves: 129S6/SvEvTac * Black Swiss * C57BL/6 * CBA/J * SJL	MGI:5297841
cn14	Nkx2-2^tm2.1Suss/Nkx2-2^tm2.1Suss Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor^+ Tg(Pdx1-cre/Esr1*)#Dam/0	involves: 129S6/SvEvTac * Black Swiss * C57BL/6 * CBA * SJL	MGI:5297840
cn15	Adamts9^tm1.1Cvrk/Adamts9^tm1.1Cvrk Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor^+ Tg(Mitf-cre)7114Gsb/0	involves: 129S6/SvEvTac * C3HeB/FeJ * C57BL/6N * CBA	MGI:6163991
cn16	Grin1^tm1c(EUCOMM)Wtsi/Grin1^tm1c(EUCOMM)Wtsi Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor^+ Tg(Slc6a4-cre)ET127Gsat/0	involves: 129S6/SvEvTac * C57BL/6 * FVB/N * SJL	MGI:5485191
cn17	Wnt1^tm1.1Mze/Wnt1^tm1.1Mze Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor^+ Shh^tm1(EGFP/cre)Cjt/Shh^+	involves: 129S6/SvEvTac * C57BL/6N	MGI:5495282
cn18	Capzb^tm1c(EUCOMM)Wtsi/Capzb^tm1c(EUCOMM)Wtsi Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor^+ Tg(Atoh1-cre)1Bfri/0	involves: 129S6/SvEvTac * C57BL/6N * CBA * SJL	MGI:6098730
cn19	Mc4r^tm2Lowl/Mc4r^tm2Lowl Chat^tm1(cre)Lowl/Chat^+ Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor^+	involves: 129S6/SvEvTac * C57BL/6NCr	MGI:5484737
cn20	Gt(ROSA)26Sor^tm1(ACTB-Map2k5*/EGFP)Zxi/Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze Tg(Nes-cre/Esr1*)4Ynj/0	involves: 129S6/SvEvTac * C57BL/6NCr	MGI:5605720
cn21	Gm30731^tm1.1Dalm/Gm30731^tm1.1Dalm Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor^+	involves: 129S6/SvEvTac * C57BL/6NCrl	MGI:6385158
cn22	Vgll4^tm1b(EUCOMM)Hmgu/Vgll4^tm1c(EUCOMM)Hmgu Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor^+ Tg(Tek-cre)1Ywa/0	involves: 129S6/SvEvTac * C57BL/6NCrl * CBA * SJL	MGI:6360909
cn23	Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor^+ Rr271^em1Mgn/Rr271^+ Sox17^tm2(EGFP/cre)Mgn/Sox17^+	involves: 129S6/SvEvTac * C57BL/6NCrl * CD-1	MGI:7339251
cn24	Wnt1^tm1.1Mze/Wnt1^tm1.1Mze Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor^+ Tg(Wnt1-cre/ERT)1Alj/0	involves: 129S6/SvEvTac * C57BL/6N * Swiss Webster	MGI:5495281
cn25	Braf^tm1Mmcm/Braf^+ Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor^+ Tg(Mitf-cre)7114Gsb/0	STOCK Braf^tm1Mmcm Gt(ROSA)26Sor^tm14(CAG-tdTomato)Hze Tg(Mitf-cre)7114Gsb/Cvrk	MGI:6792072

Genotype
MGI:4436847

ht1

• Allelic Composition: Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6NCr

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

normal phenotype

no abnormal phenotype detected ( J:155793 )

• mice are viable and fertile; used for cre reporter expression analysis

Genotype
MGI:6792058

cn2

• Allelic Composition: Gt(ROSA)26Sor^{tm1(GNAQ*)Cvrk}/Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}; Tg(Mitf-cre)7114Gsb/0
• Genetic Background: C3FeJ.Cg-Gt(ROSA)26Sor^{tm1(GNAQ*)Cvrk}/Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze} Tg(Mitf-cre)7114Gsb/Cvrk

cellular

abnormal cell physiology ( J:312561 )

• when cultured on fibronectin-coated plates, inter-follicular epidermis melanocytes exhibit reversable increased survival compared with wild-type mice

• impaired melanocyte survival and production of long, breakable and fragmentable dendrites when co-cultured with inter-follicular epidermis

• however, melanocytes exhibit normal migration and extension/retraction of protrusions when co-cultured with inter-follicular epidermis

abnormal melanocyte proliferation ( J:312561 )

• impaired proliferation when melanocytes are co-cultured with inter-follicular epidermis

integument

abnormal epidermal pigmentation ( J:312561 )

abnormal tail pigmentation ( J:312561 )

pigmentation

abnormal melanocyte proliferation ( J:312561 )

• impaired proliferation when melanocytes are co-cultured with inter-follicular epidermis

abnormal epidermal pigmentation ( J:312561 )

abnormal tail pigmentation ( J:312561 )

abnormal melanocyte morphology ( J:312561 )

• more dendritic morphology with increased protrusions per cell

• some cells in culture adopt a round shape unlike wild-type cells

• melanocytes grown with mouse embryonic fibroblasts exhibit larger and irregular shapes compared with wild-type cells

abnormal melanocyte number ( J:312561 )

hypopigmentation ( J:312561 )

limbs/digits/tail

abnormal tail pigmentation ( J:312561 )

Genotype
MGI:5495280

cn3

• Allelic Composition: Wnt1^tm1.1Mze/Wnt1^tm1.1Mze; Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/Gt(ROSA)26Sor⁺; En1^tm2(cre)Wrst/En1⁺
• Genetic Background: involves: 129 * C57BL/6N

nervous system

abnormal rhombomere morphology ( J:194842 )

• rhombomere 1 is diminished with only a small domain adjacent to axonal bundles connected to the trigeminal ganglia

• dorsal rhombomere 1 is severely depleted but the ventral portion is less severely affected

abnormal midbrain morphology ( J:194842 )

• substantial depletion of the En1 lineage derived mesencephalon at E12.5

• dorsal mesencephalon is severely depleted but the ventral portion is less severely affected

abnormal hindbrain morphology ( J:194842 )

• severe truncation of the lateral anterior hindbrain

abnormal innervation ( J:194842 )

• aberrantly patterned whisker fields innervated by serotonergic neurons

decreased neuronal precursor cell number ( J:194842 )

• absence of LMX1a+ progenitors throughout the medial-lateral extent of the ventral mesencephalon and decreased numbers in the ventral diencephalon

decreased neuron number ( J:194842 )

• only a small disorganized cohort of TH+ MbDA neurons remain at E8.5

embryo

abnormal rhombomere morphology ( J:194842 )

• rhombomere 1 is diminished with only a small domain adjacent to axonal bundles connected to the trigeminal ganglia

• dorsal rhombomere 1 is severely depleted but the ventral portion is less severely affected

Genotype
MGI:6307011

cn4

• Allelic Composition: Celf2^tm1Yjin/Celf2^tm1Yjin; Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/Gt(ROSA)26Sor⁺; Pvalb^tm1(cre)Arbr/Pvalb⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S6/SvEvTac * BALB/c * C57BL/6NCrl

nervous system

abnormal neuron physiology ( J:269731 )

• reduced adult dorsal root ganglia regeneration following sciatic nerve crush injury

Genotype
MGI:5896991

cn5

• Allelic Composition: Ednrb^tm1Nrd/Ednrb^tm1Nrd; Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/Gt(ROSA)26Sor⁺; H2az2^{Tg(Wnt1-cre)11Rth}/H2az2⁺
• Genetic Background: involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * C57BL/6 * CBA/J

digestive/alimentary system

large intestinal inflammation ( J:233811 )

• mice develop intestinal inflammation in both the proximal and mid-colon by P26-29

• however, no inflammation is seen at earlier time points on in the small intestine

hematopoietic system

abnormal mature B cell number ( J:233811 )

• mature B-lymphocytes are reduced in Peyers patches and are enriched in the spleen

decreased B cell number ( J:233811 )

• the proportion of total B-lymphocytes in Peyers patches is decreased to about 80% of levels seen in controls, indicating a 3.6-fold reduction in the number of B cells

• mice show a decrease of B-lymphocytes in the germinal centers of spleens and a decrease of B-lymphocytes within the marginal zones

• however, no differences in pre/pro-B lymphocyte and mature B lymphocyte populations at P21 in the bone marrow

decreased germinal center B cell number ( J:233811 )

• mice show a decrease of B-lymphocytes in the germinal centers of spleens

abnormal spleen morphology ( J:233811 )

• mice exhibit splenic lymphopenia

decreased marginal zone B cell number ( J:233811 )

• mice show a decrease of B-lymphocytes within the marginal zones

decreased spleen red pulp amount ( J:233811 )

small spleen ( J:233811 )

• spleens in P21-P24 mice are smaller in size

decreased spleen weight ( J:233811 )

• spleens weigh less than those of controls as a proportion of the total body weight

decreased spleen white pulp amount ( J:233811 )

abnormal splenic cell ratio ( J:233811 )

• decrease in the proportion of total (B220+) B-lymphocytes and in the numbers of total B lymphocytes in spleens

• increase in the proportion of mature B-lymphocytes in the spleen, although numbers are decreased

decreased IgA level ( J:233811 )

• secretory IgA is decreased in the small intestine

• however, no differences in secretory IgA are seen in the nasal airway lavage or bronchoalveolar lavage and no differences in small bowel luminal IgM levels are seen

immune system

large intestinal inflammation ( J:233811 )

• mice develop intestinal inflammation in both the proximal and mid-colon by P26-29

• however, no inflammation is seen at earlier time points on in the small intestine

abnormal mature B cell number ( J:233811 )

• mature B-lymphocytes are reduced in Peyers patches and are enriched in the spleen

decreased B cell number ( J:233811 )

• the proportion of total B-lymphocytes in Peyers patches is decreased to about 80% of levels seen in controls, indicating a 3.6-fold reduction in the number of B cells

• mice show a decrease of B-lymphocytes in the germinal centers of spleens and a decrease of B-lymphocytes within the marginal zones

• however, no differences in pre/pro-B lymphocyte and mature B lymphocyte populations at P21 in the bone marrow

decreased germinal center B cell number ( J:233811 )

• mice show a decrease of B-lymphocytes in the germinal centers of spleens

abnormal spleen morphology ( J:233811 )

• mice exhibit splenic lymphopenia

decreased marginal zone B cell number ( J:233811 )

• mice show a decrease of B-lymphocytes within the marginal zones

decreased spleen red pulp amount ( J:233811 )

small spleen ( J:233811 )

• spleens in P21-P24 mice are smaller in size

decreased spleen weight ( J:233811 )

• spleens weigh less than those of controls as a proportion of the total body weight

decreased spleen white pulp amount ( J:233811 )

abnormal splenic cell ratio ( J:233811 )

• decrease in the proportion of total (B220+) B-lymphocytes and in the numbers of total B lymphocytes in spleens

• increase in the proportion of mature B-lymphocytes in the spleen, although numbers are decreased

decreased IgA level ( J:233811 )

• secretory IgA is decreased in the small intestine

• however, no differences in secretory IgA are seen in the nasal airway lavage or bronchoalveolar lavage and no differences in small bowel luminal IgM levels are seen

abnormal Peyer's patch morphology ( J:233811 )

• Peyers patches are hypocellular and exhibit B-cell lymphopenia

small Peyer's patches ( J:233811 )

• Peyers patches are small in size in P21-P24 mice but have normal architecture

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Hirschsprung's disease		DOID:10487	OMIM:600156 OMIM:606874 OMIM:606875 OMIM:608462 OMIM:611644	J:233811

Genotype
MGI:6269398

cn6

• Allelic Composition: Ednrb^tm1Nrd/Ednrb^tm1Nrd; Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/Gt(ROSA)26Sor⁺; Tg(Tyr-cre/ERT2)13Bos/0
• Genetic Background: involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * C57BL/6J

integument

abnormal coat/hair pigmentation ( J:231435 )

• following induction of Cre-mediated recombination by TAM treatment at 3 weeks of age (1st telogen), mice show a noticeable hair-graying phenotype by the 2nd telogen; hair graying persists through the next hair cycle (3rd telogen), unlike in control mice

abnormal hair follicle melanocyte morphology ( J:231435 )

• following TAM treatment at 3 weeks of age (1st telogen), mice exhibit unpigmented hair follicles that contain fewer differentiated melanocytes in the bulb by anagen IV

absent hair follicle melanin granules ( J:231435 )

• following TAM treatment at 3 weeks of age (1st telogen), mice exhibit unpigmented hair follicles unlike control mice

reduced hair shaft melanin granule number ( J:231435 )

• following TAM treatment at 3 weeks of age (1st telogen), >65% of hair shafts lack melanin, leading to a hair-graying phenotype at the 2nd and 3rd telogen

pigmentation

abnormal melanocyte proliferation ( J:231435 )

• following TAM treatment at 3 weeks of age (1st telogen), melanocyte stem cells (McSCs) in unpigmented hair follicles show less BrdU incorporation than those in pigmented hair follicles of control mice at anagen III

abnormal coat/hair pigmentation ( J:231435 )

• following induction of Cre-mediated recombination by TAM treatment at 3 weeks of age (1st telogen), mice show a noticeable hair-graying phenotype by the 2nd telogen; hair graying persists through the next hair cycle (3rd telogen), unlike in control mice

abnormal hair follicle melanocyte morphology ( J:231435 )

• following TAM treatment at 3 weeks of age (1st telogen), mice exhibit unpigmented hair follicles that contain fewer differentiated melanocytes in the bulb by anagen IV

absent hair follicle melanin granules ( J:231435 )

• following TAM treatment at 3 weeks of age (1st telogen), mice exhibit unpigmented hair follicles unlike control mice

reduced hair shaft melanin granule number ( J:231435 )

• following TAM treatment at 3 weeks of age (1st telogen), >65% of hair shafts lack melanin, leading to a hair-graying phenotype at the 2nd and 3rd telogen

decreased melanocyte number ( J:231435 )

• following TAM treatment at 3 weeks of age (1st telogen), unpigmented hair follicles contain fewer differentiated melanocytes in the bulb by anagen IV, as shown by a decreased number of tomato+ melanocytes expressing differentiation markers Dct, MITF, and S100

• % of apoptotic (Casp3+) bulb melanocytes is significantly increased relative to that in control mice at anagen VI

cellular

abnormal melanocyte proliferation ( J:231435 )

• following TAM treatment at 3 weeks of age (1st telogen), melanocyte stem cells (McSCs) in unpigmented hair follicles show less BrdU incorporation than those in pigmented hair follicles of control mice at anagen III

Genotype
MGI:7541421

cn7

• Allelic Composition: Ets1^tm2Jml/Ets1^tm2Jml; Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/Gt(ROSA)26Sor⁺; Pax3^tm1(cre)Joe/Pax3⁺
• Genetic Background: involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * C57BL/6J * C57BL/6NCrl

cardiovascular system

abnormal cardiac outflow tract development ( J:334073 )

abnormal conotruncal ridge morphology ( J:334073 )

• at E13.5, alpha-actinin staining showed that cardiac myocytes are separated from the tdTomato positive cNCCs in the OFT cushion

• by E15.5, far fewer cardiomyocytes are in contact with tdTomato positive cNCCs in the OFT cushion, indicating impaired muscularization

double outlet right ventricle ( J:334073 )

• by E15.5, cNCCs persist as a fibrous outlet septum in the setting of DORV

embryo

abnormal neural crest cell physiology ( J:334073 )

• 12.7% of explanted cultured cardiac neural crest cells (cNCCs) make cell-cell contacts versus 8.5% of control cNCCs; strikingly, 81% of those contacts fail to separate within 2 h versus only 31.2% in control cNCCs, suggesting increased cell-cell adhesion

abnormal cardiac neural crest cell migration ( J:334073 )

• at E9.5, fewer tdTomato-labeled cNCCs are detected in the developing outflow tract (OFT) relative to control embryos, suggesting a delay in cNCC migration

• at E10.5, a nearly complete absence of tdTomato cNCCs is seen in the proximal component of the OFT cushions

• lack of tdTomato cNCCs in the proximal outflow cushion is less severe at E11.5; abundant cNCCs are found in the distal and intermediate outflow cushions, but not in proximal cushions, consistent with delayed migration

• moreover, number of Pax3Cre-tdTomato expressing cells that co-express SOX10 is markedly decreased and the linear migration pattern from the neural tube toward the heart is disrupted; most of tdTomato positive-expressing cells lacking SOX10 expression are located rather peripherally

• N-cadherin staining showed upregulation of N-cadherin expression in migratory NCCs at E8.5 and E9.5

• time-lapse image analysis of explanted cultured cNCCs showed a significant decrease in migration velocity relative to controls

cellular

abnormal neural crest cell physiology ( J:334073 )

• 12.7% of explanted cultured cardiac neural crest cells (cNCCs) make cell-cell contacts versus 8.5% of control cNCCs; strikingly, 81% of those contacts fail to separate within 2 h versus only 31.2% in control cNCCs, suggesting increased cell-cell adhesion

abnormal cardiac neural crest cell migration ( J:334073 )

• at E9.5, fewer tdTomato-labeled cNCCs are detected in the developing outflow tract (OFT) relative to control embryos, suggesting a delay in cNCC migration

• at E10.5, a nearly complete absence of tdTomato cNCCs is seen in the proximal component of the OFT cushions

• lack of tdTomato cNCCs in the proximal outflow cushion is less severe at E11.5; abundant cNCCs are found in the distal and intermediate outflow cushions, but not in proximal cushions, consistent with delayed migration

• moreover, number of Pax3Cre-tdTomato expressing cells that co-express SOX10 is markedly decreased and the linear migration pattern from the neural tube toward the heart is disrupted; most of tdTomato positive-expressing cells lacking SOX10 expression are located rather peripherally

• N-cadherin staining showed upregulation of N-cadherin expression in migratory NCCs at E8.5 and E9.5

• time-lapse image analysis of explanted cultured cNCCs showed a significant decrease in migration velocity relative to controls

Genotype
MGI:5485189

cn8

• Allelic Composition: Grin1^{tm1c(EUCOMM)Wtsi}/Grin1^tm2.1Stl; Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/Gt(ROSA)26Sor⁺; Tg(Slc6a4-cre)ET127Gsat/0
• Genetic Background: involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * FVB/N * SJL
• Cell Lines: EPD0469_5_C11

nervous system

abnormal innervation ( J:193625 )

• disruption of somatic innervation during development in the absence of NMDARs at P14

Genotype
MGI:7435431

cn9

• Allelic Composition: Kras^tm4Tyj/Kras⁺; Tg(Cdh5-cre/ERT2)1Rha/0; Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6NCrl * FVB

mortality/aging

postnatal lethality ( J:312482 )

• mice administered tamoxifen at P1 show early lethality beginning at P12

cardiovascular system

cardiovascular system phenotype ( J:312482 )

N • mice administered tamoxifen at P1fail to show frequent cranial hemorrhage or cortical brain arteriovenous malformations (bAVMs) at P14 or P21

Genotype
MGI:7467130

cn10

• Allelic Composition: Ctnna1^em1Xjz/Ctnna1^tm1Efu; Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/Gt(ROSA)26Sor⁺; Tg(Pdgfb-icre/ERT2,-EGFP)1Frut/0
• Genetic Background: involves: 129S6/SvEvTac * 129X1/SvJ * C57BL/6 * C57BL/6J * C57BL/6NCrl * CBA

cardiovascular system

decreased angiogenesis ( J:328283 )

• slower growth of horizontal blood vessels in retina at age P7 after tamoxifen administration from age P1-P4

hemorrhage ( J:328283 )

• increased blood vessel leakage in retina at age P7 after tamoxifen administration from age P1-P4

vision/eye

abnormal retina development ( J:328283 )

• slower growth of horizontal blood vessels in retina at age P7 after tamoxifen administration from age P1-P4

• increased blood vessel leakage at age P7 after tamoxifen administration from age P1-P4

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
exudative vitreoretinopathy		DOID:0050535	OMIM:PS133780	J:328283

Genotype
MGI:7467113

cn11

• Allelic Composition: Ctnna1^tm1Efu/Ctnna1^tm1Efu; Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/Gt(ROSA)26Sor⁺; Tg(Pdgfb-icre/ERT2,-EGFP)1Frut/0
• Genetic Background: involves: 129S6/SvEvTac * 129X1/SvJ * C57BL/6 * C57BL/6NCrl * CBA

cardiovascular system

decreased angiogenesis ( J:328283 )

• slower growth of horizontal blood vessels in retina at age P3 during tamoxifen administration from age P1-P4

• slower growth of horizontal blood vessels in retina at age P9 after tamoxifen administration from age P1-P4

• delayed growth of vertical blood vessels in superficial retina vascular plexus at age P9 after tamoxifen administration from age P1-P

• lack of vertical secondary and tertiary vessels in retina at age P9 after tamoxifen administration from age P1-P4

• defects of vascular growth into deeper layers of retina at age P9 after tamoxifen administration from age P1-P4

• defects in periphery of superficial retina vascular plexus at age P13 after tamoxifen administration from age P6

• fewer vessels in retina OPL and minimal vessels in retina IPL at age P13 after tamoxifen administration from age P6

increased angiogenesis ( J:328283 )

• enlarged superficial vessels in retina at age P9 after tamoxifen administration from age P1-P4

• enlarged blood vessels in brain at age P9 after tamoxifen administration from age P1-P4

hemorrhage ( J:328283 )

• in eyes after tamoxifen administration from age P1-P4

impaired blood-brain barrier function ( J:328283 )

• extensive blood leakage in brain at age P9 after tamoxifen administration from age P1-P4

vision/eye

abnormal retina development ( J:328283 )

• slower growth of horizontal blood vessels at age P3 during tamoxifen administration from age P1-P4

• slower growth of horizontal blood vessels and enlarged superficial vessels at age P9 after tamoxifen administration from age P1-P4

• delayed growth of vertical blood vessels in superficial retina vascular plexus at age P9 after tamoxifen administration from age P1-P4

• lack of vertical secondary and tertiary vessels at age P9 after tamoxifen administration from age P1-P4

• defects of vascular growth into deeper layers at age P9 after tamoxifen administration from age P1-P4

• defects in periphery of superficial retina vascular plexus at age P13 after tamoxifen administration from age P6

• fewer vessels in OPL and minimal vessels in IPL at age P13 after tamoxifen administration from age P6

• increased blood vessel leakage at age P9 after tamoxifen administration from age P1-P4

persistence of hyaloid vascular system ( J:328283 )

• slower regression after tamoxifen administration from age P1-P4

microphthalmia ( J:328283 )

• after tamoxifen administration from age P1-P4

mortality/aging

postnatal lethality, complete penetrance ( J:328283 )

• most mice die by age P9 after tamoxifen administration from age P1-P4

• mice die by age P13-P14 after tamoxifen administration from age P6

nervous system

impaired blood-brain barrier function ( J:328283 )

• extensive blood leakage in brain at age P9 after tamoxifen administration from age P1-P4

growth/size/body

decreased body size ( J:328283 )

• after tamoxifen administration from age P1-P4

slow postnatal weight gain ( J:328283 )

• after tamoxifen administration from age P1-P4

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
exudative vitreoretinopathy		DOID:0050535	OMIM:PS133780	J:328283

Genotype
MGI:5569627

cn12

• Allelic Composition: Htr2c^tm2Jke/Y; Tg(Pomc1-cre)16Lowl/0; Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S6/SvEvTac * 129X1/SvJ * C57BL/6 * FVB/N

nervous system

abnormal nervous system electrophysiology ( J:207704 )

• ability of the serotonin receptor 2C agonist mCPP to depolarized Pomc-expressing neurons is abolished in mutants

Genotype
MGI:5297841

cn13

• Allelic Composition: Nkx2-2^tm2.1Suss/Nkx2-2^tm2.1Suss; Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/Gt(ROSA)26Sor⁺; Tg(Ins2-cre)23Herr/0
• Genetic Background: involves: 129S6/SvEvTac * Black Swiss * C57BL/6 * CBA/J * SJL

endocrine/exocrine glands

abnormal pancreatic beta cell differentiation ( J:177838 )

• beta cells are reprogrammed to alpha cells

cellular

abnormal pancreatic beta cell differentiation ( J:177838 )

• beta cells are reprogrammed to alpha cells

Genotype
MGI:5297840

cn14

• Allelic Composition: Nkx2-2^tm2.1Suss/Nkx2-2^tm2.1Suss; Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/Gt(ROSA)26Sor⁺; Tg(Pdx1-cre/Esr1*)#Dam/0
• Genetic Background: involves: 129S6/SvEvTac * Black Swiss * C57BL/6 * CBA * SJL

endocrine/exocrine glands

abnormal pancreatic beta cell differentiation ( J:177838 )

• mice treated with tamoxifen at 3 weeks of age exhibit beta cells to alpha cells reprogramming

cellular

abnormal pancreatic beta cell differentiation ( J:177838 )

• mice treated with tamoxifen at 3 weeks of age exhibit beta cells to alpha cells reprogramming

Genotype
MGI:6163991

cn15

• Allelic Composition: Adamts9^tm1.1Cvrk/Adamts9^tm1.1Cvrk; Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/Gt(ROSA)26Sor⁺; Tg(Mitf-cre)7114Gsb/0
• Genetic Background: involves: 129S6/SvEvTac * C3HeB/FeJ * C57BL/6N * CBA

cellular

increased melanoblast apoptosis ( J:262498 )

• in some dTomato-positive tail melanoblasts at P0

embryo

increased melanoblast apoptosis ( J:262498 )

• in some dTomato-positive tail melanoblasts at P0

abnormal melanoblast morphology ( J:262498 )

• some dTomato-positive melanoblasts exhibit fragmentating indicating cell death unlike in control mice

nervous system

abnormal melanoblast morphology ( J:262498 )

• some dTomato-positive melanoblasts exhibit fragmentating indicating cell death unlike in control mice

Genotype
MGI:5485191

cn16

• Allelic Composition: Grin1^{tm1c(EUCOMM)Wtsi}/Grin1^{tm1c(EUCOMM)Wtsi}; Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/Gt(ROSA)26Sor⁺; Tg(Slc6a4-cre)ET127Gsat/0
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6 * FVB/N * SJL
• Cell Lines: EPD0469_5_C11

nervous system

abnormal innervation ( J:193625 )

• disruption of somatic innervation during development in the absence of NMDARs at P14

Genotype
MGI:5495282

cn17

• Allelic Composition: Wnt1^tm1.1Mze/Wnt1^tm1.1Mze; Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/Gt(ROSA)26Sor⁺; Shh^{tm1(EGFP/cre)Cjt}/Shh⁺
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6N

nervous system

premature neuronal precursor differentiation ( J:194842 )

• significant increase of the number of differentiated MbDA neurons at E11.5

• significant increase in the number of Ki67+ progenitors in the differentiating zone in medial planes

abnormal midbrain morphology ( J:194842 )

• depletion of medial MbDA neurons and expansion of more laterally positioned MbDA neurons at E12.5

decreased neuron number ( J:194842 )

• depletion of medial MbDA neurons

cellular

premature neuronal precursor differentiation ( J:194842 )

• significant increase of the number of differentiated MbDA neurons at E11.5

• significant increase in the number of Ki67+ progenitors in the differentiating zone in medial planes

Genotype
MGI:6098730

cn18

• Allelic Composition: Capzb^{tm1c(EUCOMM)Wtsi}/Capzb^{tm1c(EUCOMM)Wtsi}; Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/Gt(ROSA)26Sor⁺; Tg(Atoh1-cre)1Bfri/0
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6N * CBA * SJL
• Cell Lines: EPD0105_5_A09

hearing/vestibular/ear

abnormal cochlea morphology ( J:246055 )

• increased actin aggregation in the adherens-junction region and expansion of the apical surface

decreased cochlear hair cell stereocilia number ( J:246055 )

• no distinguishable stereocilia

cochlear hair cell degeneration ( J:246055 )

• reduction in stereocilia diameter and length eventually followed by disappearance

abnormal cuticular plate morphology ( J:246055 )

• ruptures

abnormal vestibular hair cell stereociliary bundle morphology ( J:246055 )

• disrupted hair cell in some bundles

short vestibular hair cell stereocilia ( J:246055 )

• with decreased width

nervous system

decreased cochlear hair cell stereocilia number ( J:246055 )

• no distinguishable stereocilia

cochlear hair cell degeneration ( J:246055 )

• reduction in stereocilia diameter and length eventually followed by disappearance

abnormal vestibular hair cell stereociliary bundle morphology ( J:246055 )

• disrupted hair cell in some bundles

short vestibular hair cell stereocilia ( J:246055 )

• with decreased width

Genotype
MGI:5484737

cn19

• Allelic Composition: Mc4r^tm2Lowl/Mc4r^tm2Lowl; Chat^tm1(cre)Lowl/Chat⁺; Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6NCr

nervous system

nervous system phenotype ( J:193452 )

N • biophysical properties of cholinergic neurons are normal

abnormal nervous system electrophysiology ( J:193452 )

• melanotan II fails to hyperpolarize membrane potentials of all dorsal motor nucleus vagal cholinergic neurons

• similar results with Mc4r agonist THIQ

Genotype
MGI:5605720

cn20

• Allelic Composition: Gt(ROSA)26Sor^{tm1(ACTB-Map2k5*/EGFP)Zxi}/Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}; Tg(Nes-cre/Esr1*)4Ynj/0
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6NCr

nervous system

nervous system phenotype ( J:206948 )

N • no change in the volume of the granule cell layer in the dentate gyrus or in the number of radial glia-like adult neural stem cells indicating no affect on the adult neural stem cell pool

abnormal dentate gyrus morphology ( J:206948 )

• increase in the number of NeuN+ neurons in tamoxifen treated mice at 3 weeks and 7 weeks of age

abnormal dendrite morphology ( J:206948 )

• average primary dendritic length and number of dendritic crossings are increased in the dentate gyrus in tamoxifen treated mice

abnormal dendritic spine morphology ( J:206948 )

• increase in spine density in the dentate gyrus in tamoxifen treated mice

Genotype
MGI:6385158

cn21

• Allelic Composition: Gm30731^tm1.1Dalm/Gm30731^tm1.1Dalm; Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6NCrl

nervous system

abnormal neuronal stem cell physiology ( J:281278 )

• cell-autonomous increased neurogenesis following injection of a cre-expressing adenovirus into lateral ventricles at E13.5

Genotype
MGI:6360909

cn22

• Allelic Composition: Vgll4^{tm1b(EUCOMM)Hmgu}/Vgll4^{tm1c(EUCOMM)Hmgu}; Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/Gt(ROSA)26Sor⁺; Tg(Tek-cre)1Ywa/0
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6NCrl * CBA * SJL

cardiovascular system

abnormal heart development ( J:273437 )

• non-cell autonomous, enhanced proliferation of endothelial-derived valvar interstitial cells leading to valve thickening

Genotype
MGI:7339251

cn23

• Allelic Composition: Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/Gt(ROSA)26Sor⁺; Rr271^em1Mgn/Rr271⁺; Sox17^{tm2(EGFP/cre)Mgn}/Sox17⁺
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6NCrl * CD-1

digestive/alimentary system

truncated foregut ( J:328045 )

• absence of ventral pancreato-biliary bud

embryo

failure of initiation of embryo turning ( J:328045 )

decreased embryo size ( J:328045 )

• growth retardation from E9.5

• degraded posterior body trunk at E9.5

growth/size/body

decreased embryo size ( J:328045 )

• growth retardation from E9.5

• degraded posterior body trunk at E9.5

Genotype
MGI:5495281

cn24

• Allelic Composition: Wnt1^tm1.1Mze/Wnt1^tm1.1Mze; Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/Gt(ROSA)26Sor⁺; Tg(Wnt1-cre/ERT)1Alj/0
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6N * Swiss Webster

nervous system

abnormal midbrain morphology ( J:194842 )

• following tamoxifen treatment at E8.5, the ventral mesencephalon is smaller and has an abnormal notch at E12.5

• depletion of TH+ neurons in the medial ventral mesencephalon and an increase in TH+ neurons in the off-midline plane in 2 of 4 embryos at E12.5

• tamoxifen treatment at E10.5 does not produce an overt phenotype in the mesencephalon

Genotype
MGI:6792072

cn25

• Allelic Composition: Braf^tm1Mmcm/Braf⁺; Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/Gt(ROSA)26Sor⁺; Tg(Mitf-cre)7114Gsb/0
• Genetic Background: STOCK Braf^tm1Mmcm Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze} Tg(Mitf-cre)7114Gsb/Cvrk

cellular

abnormal cell physiology ( J:312561 )

• when cultured on fibronectin-coated plates, inter-follicular epidermis melanocytes exhibit increased survival compared with wild-type mice

integument

increased tail pigmentation ( J:312561 )

limbs/digits/tail

increased tail pigmentation ( J:312561 )

pigmentation

increased tail pigmentation ( J:312561 )