Phenotypes associated with this allele

• Allele Symbol: Tal1^tm2Wehi
• Allele Name: targeted mutation 2, Walter and Eliza Hall, Institute of Medical Research
• Allele ID: MGI:1858004
• Summary: 2 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Tal1^tm2Wehi/Tal1^tm2Wehi	involves: 129S1/Sv * C57BL/6	MGI:2174754
cn2	Tal1^tm3Wehi/Tal1^tm2Wehi Tg(Mx1-cre)1Cgn/0	involves: 129S1/Sv * C57BL/6 * CBA	MGI:2450773

Genotype
MGI:2174754

hm1

• Allelic Composition: Tal1^tm2Wehi/Tal1^tm2Wehi
• Genetic Background: involves: 129S1/Sv * C57BL/6

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

mortality/aging

embryonic lethality during organogenesis, complete penetrance ( J:58825 )

• homozygotes die by about E9.5 due to absolute anemia

embryo

absent vitelline blood vessels ( J:58825 )

• at E9.5, mutant yolk sacs lack large branching vitelline vessels

disorganized yolk sac vascular plexus ( J:58825 )

• by E8, mutant yolk sacs exhibit a disorganized network of fine vascular channels

embryonic growth arrest ( J:58825 )

• at E9.5, preterminal homozygotes are severely growth-retarded

absent visceral yolk sac blood islands ( J:58825 )

• at E8.5, mutant yolk sacs display bloodless channels; PECAM-1 staining is restricted to the endothelium

abnormal embryonic hematopoiesis ( J:58825 )

• homozygotes exhibit failure of yolk sac hematopoiesis, with no erythrocytes found in embryonic vessels

cardiovascular system

abnormal blood vessel morphology ( J:58825 )

• at E8.5, homozygotes display reduced cerebral vasculature with dilated intraembryonic vessels

• at E9.0, incomplete somitic vessels appear to undergo apoptosis resulting in loss of vascular architecture by E9.5

dilated dorsal aorta ( J:58825 )

• at E8.5, homozygotes exhibit dilated dorsal aortae

absent vitelline blood vessels ( J:58825 )

• at E9.5, mutant yolk sacs lack large branching vitelline vessels

disorganized yolk sac vascular plexus ( J:58825 )

• by E8, mutant yolk sacs exhibit a disorganized network of fine vascular channels

abnormal vein morphology ( J:58825 )

• at E8.5, homozygotes display dilated cardinal and perineural veins

abnormal heart development ( J:58825 )

delayed heart looping ( J:58825 )

• at E8.5, the mutant heart is still a straight tube as a result of delayed cardiac looping

pericardial edema ( J:58825 )

• at E8.5, homozygotes display significant pericardial edema

distended pericardium ( J:58825 )

• at E8.5, homozygotes exhibit dilated pericardial sacs

hematopoietic system

abnormal embryonic hematopoiesis ( J:58825 )

• homozygotes exhibit failure of yolk sac hematopoiesis, with no erythrocytes found in embryonic vessels

anemia ( J:58825 )

• at E8.5-E9, homozygotes exhibit absolute anemia leading to hypoxia

homeostasis/metabolism

pericardial edema ( J:58825 )

• at E8.5, homozygotes display significant pericardial edema

hypoxia ( J:58825 )

• by E9.0, homozygotes display widespread intraembryonic hypoxic cell death

nervous system

increased neuron apoptosis ( J:58825 )

• at E8.5, homozygotes display an increased number of apoptotic cells in the neural tube, probably secondary to hypoxia

cellular

increased neuron apoptosis ( J:58825 )

• at E8.5, homozygotes display an increased number of apoptotic cells in the neural tube, probably secondary to hypoxia

Genotype
MGI:2450773

cn2

• Allelic Composition: Tal1^tm3Wehi/Tal1^tm2Wehi; Tg(Mx1-cre)1Cgn/0
• Genetic Background: involves: 129S1/Sv * C57BL/6 * CBA

hematopoietic system

abnormal erythropoiesis ( J:81826 )

• at day 6 after PI-PC treatment, mutant mice show impaired erythropoiesis in bone marrow and spleen; a 4-fold reduction of mature erythroid cells is noted in speen

anemia ( J:81826 )

• both mutant and control mice show a 25% reduction in hematocrit levels at 6 days after PI-PC treatment; however, control animals are able to normalize this defect 1 week later, whereas mutant mice remain anemic

impaired hematopoiesis ( J:81826 )

• adult mutant mice exhibit impaired megakaryopoiesis and erythropoiesis with loss of early progenitor cells in both lineages

decreased bone marrow cell number ( J:81826 )

• mutants display a 50% reduction in total bone marrow cellularity relative to control mice

abnormal megakaryocyte morphology ( J:81826 )

• megakaryocytes from mutant bone marrows are larger (~2-fold increase in diameter) and appear dysplastic with hyperlobulated nuclei

• megakaryocytes are virtually absent from the spleens of mutant mice; however, megakaryocytes in deleted bone marrows retain the ability to shed platelets in response to thrombocytopenia

• in mutant bone marrow, CFU-S12 colonies are reduced 2-fold and appear smaller and pale with no erythroid or megakaryocytic component

abnormal megakaryocyte progenitor cell morphology ( J:81826 )

• in vitro, mutant bone marrows and spleens are devoid of megakaryocyte progenitors

abnormal proerythroblast morphology ( J:81826 )

• at 6 days after PI-PC treatment, mutant bone marrows and spleens are devoid of erythroid progenitors (BFU-E)

• in contrast, the frequency and behavior of myeloid CFCs is not significantly affected

thrombocytopenia ( J:81826 )

• after 6 days and 3 injections of PI-PC, mutant mice continue to display decreased platelet counts whereas increased megakaryocytopoiesis in the spleen has normalized platelet counts in control mice

• notably, mutant mice do recover completely from the acute fall in their white cell count

abnormal splenic cell ratio ( J:81826 )

• megakaryocytes are virtually absent from the spleens of mutant mice

immune system

abnormal splenic cell ratio ( J:81826 )

• megakaryocytes are virtually absent from the spleens of mutant mice

skeleton

abnormal bone marrow morphology ( J:81826 )

• flushed bone marrow samples from mutant mice are pale relative to control samples