All Phenotypes Gt(ROSA)26Sor<tm1(cre/ERT2)Alj> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Elavl1^tm1Thla/Elavl1^tm1Thla Gt(ROSA)26Sor^{tm1(cre/ERT2)Alj}/Gt(ROSA)26Sor⁺	involves: 129	MGI:4414940
cn2	En1^tm1Alj/En1^tm8.1Alj En2^tm1Alj/En2^tm7.1Alj Gt(ROSA)26Sor^{tm1(cre/ERT2)Alj}/Gt(ROSA)26Sor⁺	involves: 129S1/Sv * 129S2/SvPas * 129S6/SvEvTac * 129X1/SvJ * Swiss Webster	MGI:4421427
cn3	En1^tm1Alj/En1^tm8.1Alj En2^tm6Alj/En2⁺ Gt(ROSA)26Sor^{tm1(cre/ERT2)Alj}/Gt(ROSA)26Sor⁺	involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * Swiss Webster	MGI:4421456
cn4	En2^tm1Alj/En2^tm6Alj Gt(ROSA)26Sor^{tm1(cre/ERT2)Alj}/Gt(ROSA)26Sor⁺	involves: 129S2/SvPas * 129S6/SvEvTac * Swiss Webster	MGI:4421426
cn5	En1^tm1Alj/En1^tm8.1Alj En2^tm1Alj/En2^tm6Alj Gt(ROSA)26Sor^{tm1(cre/ERT2)Alj}/Gt(ROSA)26Sor⁺	involves: 129S2/SvPas * 129S6/SvEvTac * Swiss Webster	MGI:4421433
cn6	En2^tm5.1Alj/En2^tm5.1Alj Gt(ROSA)26Sor^{tm1(cre/ERT2)Alj}/Gt(ROSA)26Sor⁺	involves: 129S2/SvPas * Swiss Webster	MGI:4421418
cn7	Egln1^tm2Fong/Egln1^tm2Fong Gt(ROSA)26Sor^{tm1(cre/ERT2)Alj}/Gt(ROSA)26Sor⁺	involves: 129S6/SvEvTac * C57BL/6	MGI:3783535
cn8	En1^tm8.1Alj/En1⁺ En2^tm6Alj/En2⁺ Gt(ROSA)26Sor^{tm1(cre/ERT2)Alj}/Gt(ROSA)26Sor⁺	involves: 129S6/SvEvTac * Swiss Webster	MGI:4421432

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

Cachexic phenotype of Elavl1^tm1Thla/Elavl1^tm1Thla Gt(ROSA)26Sor^{tm1(cre/ERT2)Alj}/Gt(ROSA)26Sor⁺ mice observed 4 days after tamoxifen administration

mortality/aging

premature death ( J:155109 )

• 10 days after tamoxifen treatment

immune system

increased T cell apoptosis ( J:155109 )

• following tamoxifen treatment, double positive T cells in the thymus exhibit increased apoptosis and necrosis and decreased proliferation compared with T cells from Elavl1^tm1Hela homozygotes

thymus hypoplasia ( J:155109 )

• following tamoxifen treatment

decreased leukocyte cell number ( J:155109 )

• 65% 4 days following tamoxifen treatment

decreased double-positive T cell number ( J:155109 )

• following tamoxifen treatment

abnormal myeloid leukocyte morphology ( J:155109 )

• following tamoxifen treatment, myeloid cell numbers are decreased compared to in Elavl1^tm1Hela homozygotes

decreased granulocyte number ( J:155109 )

• 4 days following tamoxifen treatment

increased granulocyte number ( J:155109 )

• 2-fold following tamoxifen treatment

spleen hypoplasia ( J:155109 )

• following tamoxifen treatment

abnormal B cell physiology ( J:155109 )

• following tamoxifen treatment, early B cells exhibit increased apoptosis and necrosis and decreased proliferation compared with B cells from Elavl1^tm1Hela homozygotes

decreased B cell apoptosis ( J:155109 )

• following tamoxifen treatment, early B cells exhibit increased apoptosis and necrosis and decreased proliferation compared with B cells from Elavl1^tm1Hela homozygotes

lymph node hypoplasia ( J:155109 )

• following tamoxifen treatment

hematopoietic system

increased T cell apoptosis ( J:155109 )

• following tamoxifen treatment, double positive T cells in the thymus exhibit increased apoptosis and necrosis and decreased proliferation compared with T cells from Elavl1^tm1Hela homozygotes

thymus hypoplasia ( J:155109 )

• following tamoxifen treatment

abnormal definitive hematopoiesis ( J:155109 )

• bone marrow from tamoxifen-treated mice exhibits decreased myeloerythroid colonies on methylcellulose compared with bone marrow from Elavl1^tm1Hela homozygotes

decreased common myeloid progenitor cell number ( J:155109 )

• following tamoxifen treatment

decreased bone marrow cell number ( J:155109 )

• following tamoxifen treatment, total bone marrow cell numbers and bone marrow cellularity of immature cells are decreased compared to in Elavl1^tm1Hela homozygotes

decreased erythroid progenitor cell number ( J:155109 )

• following tamoxifen treatment

decreased leukocyte cell number ( J:155109 )

• 65% 4 days following tamoxifen treatment

decreased double-positive T cell number ( J:155109 )

• following tamoxifen treatment

abnormal myeloid leukocyte morphology ( J:155109 )

• following tamoxifen treatment, myeloid cell numbers are decreased compared to in Elavl1^tm1Hela homozygotes

decreased granulocyte number ( J:155109 )

• 4 days following tamoxifen treatment

increased granulocyte number ( J:155109 )

• 2-fold following tamoxifen treatment

spleen hypoplasia ( J:155109 )

• following tamoxifen treatment

abnormal B cell physiology ( J:155109 )

• following tamoxifen treatment, early B cells exhibit increased apoptosis and necrosis and decreased proliferation compared with B cells from Elavl1^tm1Hela homozygotes

decreased B cell apoptosis ( J:155109 )

• following tamoxifen treatment, early B cells exhibit increased apoptosis and necrosis and decreased proliferation compared with B cells from Elavl1^tm1Hela homozygotes

digestive/alimentary system

abnormal intestinal epithelium morphology ( J:155109 )

• 2 to 3 days following tamoxifen treatment, mice exhibit massive villus atrophy and disruption of the epithelial architecture unlike Elavl1^tm1Hela homozygotes

abnormal intestinal mucosa morphology ( J:155109 )

• disrupted following tamoxifen treatment

abnormal intestinal goblet cell morphology ( J:155109 )

• following tamoxifen treatment, goblet cells are lost unlike in Elavl1^tm1Hela homozygotes

abnormal crypts of Lieberkuhn morphology ( J:155109 )

• following tamoxifen treatment, proliferation of crypt progenitor cells is decreased while apoptosis is increased unlike in Elavl1^tm1Hela homozygotes

abnormal colon morphology ( J:155109 )

• following tamoxifen treatment, apoptosis of cells in the lamina propria and epithelial cells of the colon is increased compared to in Elavl1^tm1Hela homozygotes

small intestinal villus atrophy ( J:155109 )

• 2 to 3 days following tamoxifen treatment, mice exhibit massive villus atrophy unlike Elavl1^tm1Hela homozygotes

distended stomach ( J:155109 )

• 2 to 4 days following tamoxifen treatment

intestinal obstruction ( J:155109 )

• 2 to 4 days following tamoxifen treatment the proximal intestine is devoid of food suggesting intestinal blockage

growth/size/body

cachexia ( J:155109 )

• following tamoxifen treatment

cellular

abnormal intestinal goblet cell morphology ( J:155109 )

• following tamoxifen treatment, goblet cells are lost unlike in Elavl1^tm1Hela homozygotes

decreased B cell apoptosis ( J:155109 )

• following tamoxifen treatment, early B cells exhibit increased apoptosis and necrosis and decreased proliferation compared with B cells from Elavl1^tm1Hela homozygotes

increased T cell apoptosis ( J:155109 )

• following tamoxifen treatment, double positive T cells in the thymus exhibit increased apoptosis and necrosis and decreased proliferation compared with T cells from Elavl1^tm1Hela homozygotes

decreased cell proliferation ( J:155109 )

• mouse embryonic fibroblasts treated with 4-hydoxytamoxifen exhibit decreased proliferation compared with similarly treated cells from Elavl1^tm1Hela homozygotes

endocrine/exocrine glands

abnormal crypts of Lieberkuhn morphology ( J:155109 )

• following tamoxifen treatment, proliferation of crypt progenitor cells is decreased while apoptosis is increased unlike in Elavl1^tm1Hela homozygotes

thymus hypoplasia ( J:155109 )

• following tamoxifen treatment

Allelic Composition	En1^tm1Alj/En1^tm8.1Alj En2^tm1Alj/En2^tm7.1Alj Gt(ROSA)26Sor^{tm1(cre/ERT2)Alj}/Gt(ROSA)26Sor⁺
Genetic Background	involves: 129S1/Sv * 129S2/SvPas * 129S6/SvEvTac * 129X1/SvJ * Swiss Webster

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
En1^tm1Alj mutation (2 available); any En1 mutation (32 available)
En1^tm8.1Alj mutation (1 available); any En1 mutation (32 available)
En2^tm1Alj mutation (1 available); any En2 mutation (104 available)
En2^tm7.1Alj mutation (0 available); any En2 mutation (104 available)
Gt(ROSA)26Sor^{tm1(cre/ERT2)Alj} mutation (0 available); any Gt(ROSA)26Sor mutation (942 available)

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

nervous system

abnormal cerebellar foliation ( J:156169 )

abnormal cerebellum hemisphere lobule morphology ( J:156169 )

• when given tamoxifen at E13.5 or E14. the hemisphere phenotype is more severe than in double mutants that do not express Cre

abnormal cerebellum vermis lobule morphology ( J:156169 )

• when given tamoxifen at E13.5 or E14. the vermis phenotype is more severe than in double mutants that do not express Cre

Allelic Composition	En1^tm1Alj/En1^tm8.1Alj En2^tm6Alj/En2⁺ Gt(ROSA)26Sor^{tm1(cre/ERT2)Alj}/Gt(ROSA)26Sor⁺
Genetic Background	involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * Swiss Webster

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
En1^tm1Alj mutation (2 available); any En1 mutation (32 available)
En1^tm8.1Alj mutation (1 available); any En1 mutation (32 available)
En2^tm6Alj mutation (1 available); any En2 mutation (104 available)
Gt(ROSA)26Sor^{tm1(cre/ERT2)Alj} mutation (0 available); any Gt(ROSA)26Sor mutation (942 available)

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

nervous system

abnormal cerebellar foliation ( J:156169 )

decreased anterior vermis size ( J:156169 )

• when given tamoxifen at E10.5, at P21 the anterior region (lobules I-V) is reduced and the central region (lobules VI-VII) is preferentially expanded.

abnormal cerebellum vermis lobule morphology ( J:156169 )

• when tamoxifen is given at E10.5, at P21 lobule VIII extends more laterally than normal, as do lobules I-V but only on one side

Allelic Composition	En2^tm1Alj/En2^tm6Alj Gt(ROSA)26Sor^{tm1(cre/ERT2)Alj}/Gt(ROSA)26Sor⁺
Genetic Background	involves: 129S2/SvPas * 129S6/SvEvTac * Swiss Webster

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
En2^tm1Alj mutation (1 available); any En2 mutation (104 available)
En2^tm6Alj mutation (1 available); any En2 mutation (104 available)
Gt(ROSA)26Sor^{tm1(cre/ERT2)Alj} mutation (0 available); any Gt(ROSA)26Sor mutation (942 available)

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

nervous system

abnormal cerebellar foliation ( J:156169 )

• following tamoxifen administration at E9.5 - E12.5, all or almost all display an abnormal foliation pattern similar to that in En2 null mice

abnormal cerebellum hemisphere lobule morphology ( J:156169 )

• following tamoxifen administration at E9.5 - E12.5, all or almost all display an abnormal foliation pattern similar to that in En2 null mice

abnormal cerebellum vermis lobule morphology ( J:156169 )

• following tamoxifen administration at E9.5 - E12.5, all or almost all display an abnormal foliation pattern similar to that in En2 null mice

Allelic Composition	En1^tm1Alj/En1^tm8.1Alj En2^tm1Alj/En2^tm6Alj Gt(ROSA)26Sor^{tm1(cre/ERT2)Alj}/Gt(ROSA)26Sor⁺
Genetic Background	involves: 129S2/SvPas * 129S6/SvEvTac * Swiss Webster

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
En1^tm1Alj mutation (2 available); any En1 mutation (32 available)
En1^tm8.1Alj mutation (1 available); any En1 mutation (32 available)
En2^tm1Alj mutation (1 available); any En2 mutation (104 available)
En2^tm6Alj mutation (1 available); any En2 mutation (104 available)
Gt(ROSA)26Sor^{tm1(cre/ERT2)Alj} mutation (0 available); any Gt(ROSA)26Sor mutation (942 available)

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

mortality/aging

perinatal lethality, complete penetrance ( J:156169 )

• tamoxifen treatment at E9.5, but not at E10.5, results in death at birth

nervous system

abnormal cerebellar granule cell precursor proliferation ( J:156169 )

• when tamoxifen treated at E10.5, at P2 proliferation is similar in the anterior and central lobules, unlike in wild-type mice

abnormal midbrain morphology ( J:156169 )

• a major deletion of the midbrain is seen when tamoxifen is given at E9.5, but not when given at E10.5

abnormal cerebellum morphology ( J:156169 )

• a major deletion of the medial cerebellum is seen when tamoxifen is given at E9.5 but not when given at E10.5

• when given tamoxifen at E10.5, at P14 the distinction between the vermis and the hemispheres is not apparent

abnormal cerebellum development ( J:156169 )

• when given tamoxifen at E10.5, at E12.5 the cerebellar primordium is reduced in size

• when tamoxifen treated at E10.5, development of the vermis prepyramidal fissure is delayed and the order of fissure initiation is altered

abnormal cerebellar foliation ( J:156169 )

• when given tamoxifen at E10.5, at P14 cerebellar foliation patterns are disrupted

• when given tamoxifen at E13.5 or E14.5, foliation defects in adults are less severe than when tamoxifen is given at E10.5

abnormal cerebellum external granule cell layer morphology ( J:156169 )

• when tamoxifen treated at E10.5, at E18.5 the thickness of the external granule layer was 1.5-2 times greater in the mutants than in wild types

• when tamoxifen treated at E10.5, at P2 the thickness of the external granule layer is similar in the lobules IV/V and VI unlike in wild-type mice

thin external granule cell layer ( J:156169 )

• when tamoxifen treated at E10.5, at P2 thickness is similar to that at E18.5 and thinner than in the controls.

abnormal cerebellum fissure morphology ( J:156169 )

• when given tamoxifen at E13.5 or E14.5, in adults the preculminate fissure is absent (between I-II and III) as lobules I-III are fused

• when given tamoxifen at E10.5, at P3 the depth of the primary fissure is increased relative to the intercrural fissure

abnormal cerebellum vermis morphology ( J:156169 )

decreased anterior vermis size ( J:156169 )

• when given tamoxifen at E10.5, at P14 the anterior region (lobules I-V) is reduced and the central region (lobules VI-VII) is preferentially expanded

abnormal cerebellum vermis lobule morphology ( J:156169 )

• when tamoxifen is given at E10.5, at P14, unlike in wild type, the remnants of lobules I-V extend into the hemispheres

• when tamoxifen is given at E10.5, at P14 remnants of the vermis, specific anterior and posterior regions, are maintained more laterally than in wild-type

• when given tamoxifen at E10.5, at P14 in some mutants lobule VIII is diminished more medially than lobule IX rather than the opposite as occurs in wild-type

• when tamoxifen treated at E10.5, at P2 lobules I - V are smaller and lobule VI is much larger than in wild-type

• when tamoxifen is given at E13.5 or E14.5, in adults lobule VIII is shifted posterior and fused with dorsal lobule IX

• when tamoxifen treated at E10.5, at P2 the thickness of the external granule layer is similar in the lobules IV/V and VI unlike in wild-type mice

abnormal cerebellum posterior vermis morphology ( J:156169 )

• when given tamoxifen at E10.5, at P14 lobules VI-VII occupy a greater proportion of the vermis than in wild-type

• when given tamoxifen at E10.5, at P14 lobules VIII-IX occupy a smaller proportion of the vermis than in wild-type

• when given tamoxifen at E13.5 or E14.5, in adults lobules I-III are fused into one lobule

cerebellum vermis hypoplasia ( J:156169 )

• when tamoxifen treated at E10.5, at P2 overall size of each region, and thus total number of cells, is greatly reduced

small cerebellum ( J:156169 )

• when given tamoxifen, at P3 the cerebellum is smaller compared to controls

cellular

abnormal cerebellar granule cell precursor proliferation ( J:156169 )

• when tamoxifen treated at E10.5, at P2 proliferation is similar in the anterior and central lobules, unlike in wild-type mice

Allelic Composition	En2^tm5.1Alj/En2^tm5.1Alj Gt(ROSA)26Sor^{tm1(cre/ERT2)Alj}/Gt(ROSA)26Sor⁺
Genetic Background	involves: 129S2/SvPas * Swiss Webster

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
En2^tm5.1Alj mutation (1 available); any En2 mutation (104 available)
Gt(ROSA)26Sor^{tm1(cre/ERT2)Alj} mutation (0 available); any Gt(ROSA)26Sor mutation (942 available)

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

nervous system

nervous system phenotype ( J:156169 )

N	• following tamoxifen administration at E9.5 - E12.5, foliation pattern is rescued

Allelic Composition	Egln1^tm2Fong/Egln1^tm2Fong Gt(ROSA)26Sor^{tm1(cre/ERT2)Alj}/Gt(ROSA)26Sor⁺
Genetic Background	involves: 129S6/SvEvTac * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Egln1^tm2Fong mutation (1 available); any Egln1 mutation (21 available)
Gt(ROSA)26Sor^{tm1(cre/ERT2)Alj} mutation (0 available); any Gt(ROSA)26Sor mutation (942 available)

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

mortality/aging

decreased survivor rate ( J:132720 )

• reach 90% lethality by about 90 days after tamoxifen treatment

premature death ( J:132720 )

• mice begin to die 40 days after tamoxifen treatment with 90% lethality by about 90 days after treatment

cardiovascular system

abnormal blood vessel morphology ( J:133568 )

• about 6 weeks after tamoxifen treatment major vascular branches of the ear are dilated and reddened and medium-sized blood vessels are scattered in the subendocardial layer

• after tamoxifen treatment, liver sections show an increase in large vessels

abnormal capillary morphology ( J:133568 )

• after tamoxifen treatment the trachea contains more capillaries which are more branched and enlarged

• after tamoxifen treatment capillaries amid cardiac fibers are enlarged as are capillaries in the renal glomeruli

abnormal capillary branching pattern ( J:133568 )

abnormal kidney vasculature morphology ( J:133568 )

• dilated vessels and enlarged glomerular capillaries after tamoxifen treatment

dilated liver sinusoidal space ( J:133568 )

• sinusoids are dilated after tamoxifen treatment

abnormal lung vasculature morphology ( J:133568 )

• after tamoxifen treatment the size and number of blood vessels in the lung is increased

increased angiogenesis ( J:133568 )

• after tamoxifen treatment increased numbers of blood vessels are seen in the dermal and subcutaneous layers of the ear, the trachea contains more capillaries which are more branched and enlarged, more medium sized vessels are present in the subendocardial layer of the heart, and more vessels are seen in the liver and brain

dilated vasculature ( J:133568 )

• about 6 weeks after tamoxifen treatment vessels in the ear, trachea, heart, lung, kidney cortex and glomeruli, liver

• in the lung vessel dilation is accompanied by packed erythrocytes

• in the liver central veins are about 4-times larger than in controls

hematopoietic system

enlarged spleen ( J:132720 )

abnormal definitive hematopoiesis ( J:132720 )

extramedullary hematopoiesis ( J:132720 )

• significant increase in hematopoietic stem cells in the liver and spleen after tamoxifen treatment

• increase in the number of colonies formed by spleen and liver cells in a methylcellulose colony forming assay after tamoxifen treatment

polycythemia ( J:132720 )

• after tamoxifen treatment

increased hematocrit ( J:132720 )

• dramatic increase after tamoxifen treatment

increased hemoglobin content ( J:132720 )

• after tamoxifen treatment

increased leukocyte cell number ( J:132720 )

• after tamoxifen treatment

abnormal splenic cell ratio ( J:132720 )

• increase in the number of erythroid progenitor and myeloid cells after tamoxifen treatment

liver/biliary system

abnormal liver morphology ( J:132720 )

• more strongly colored than controls after tamoxifen treatment

dilated liver sinusoidal space ( J:133568 )

• sinusoids are dilated after tamoxifen treatment

enlarged liver ( J:132720 )

renal/urinary system

abnormal kidney vasculature morphology ( J:133568 )

• dilated vessels and enlarged glomerular capillaries after tamoxifen treatment

abnormal renal glomerulus morphology ( J:133568 )

• glomeruli are enlarged and their capillaries are dilated

homeostasis/metabolism

increased circulating erythropoietin level ( J:132720 )

• 230-fold increase in serum erythropoietin levels within 2 weeks of tamoxifen treatment

immune system

enlarged spleen ( J:132720 )

increased leukocyte cell number ( J:132720 )

• after tamoxifen treatment

abnormal splenic cell ratio ( J:132720 )

• increase in the number of erythroid progenitor and myeloid cells after tamoxifen treatment

respiratory system

abnormal lung vasculature morphology ( J:133568 )

• after tamoxifen treatment the size and number of blood vessels in the lung is increased

integument

reddish skin ( J:132720 )

• erythemia is more apparent than in Egln2^tm1Fong Egln3^tm1Fong double homozygotes

growth/size/body

enlarged liver ( J:132720 )

enlarged spleen ( J:132720 )

Allelic Composition	En1^tm8.1Alj/En1⁺ En2^tm6Alj/En2⁺ Gt(ROSA)26Sor^{tm1(cre/ERT2)Alj}/Gt(ROSA)26Sor⁺
Genetic Background	involves: 129S6/SvEvTac * Swiss Webster

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
En1^tm8.1Alj mutation (1 available); any En1 mutation (32 available)
En2^tm6Alj mutation (1 available); any En2 mutation (104 available)
Gt(ROSA)26Sor^{tm1(cre/ERT2)Alj} mutation (0 available); any Gt(ROSA)26Sor mutation (942 available)

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

nervous system

abnormal cerebellar foliation ( J:156169 )

abnormal cerebellum fissure morphology ( J:156169 )

• when tamoxifen is given at E13.5 or E14.5 in adult preculminate (between I-II and III) as lobules I-III are fused

abnormal cerebellum posterior vermis morphology ( J:156169 )

• when tamoxifen is given at E10.5, at P14 lobules VI-VII occupied a greater proportion of the vermis than in wild-type

• when tamoxifen is given at E10.5, at P14 lobules VIII-IX occupied a smaller proportion of the vermis than in wild-type

• when tamoxifen is given at E13.5 or E14.5 in adult the vermis has a foliation pattern that was a milder version than that observed in tamoxifen at 10.5 mutants

• when tamoxifen is given at E13.5 or E14.5 in adult posterior region lobule VIII is shifted posterior and fused with dorsal lobule IX.

• when tamoxifen is given at E13.5 or E14.5 in adult lobules I-V and VIII/IX of the vermis were present more laterally than normal tamoxifen at E13.5 or E14.5 in adult lobules I-III were fused into one lobule

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