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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tlx1tm1Sjk
targeted mutation 1, Stanley J Korsmeyer
MGI:1857260
Summary 2 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Tlx1tm1Sjk/Tlx1tm1Sjk involves: 129S2/SvPas MGI:2668994
cx2
Tlx1tm1Sjk/Tlx1tm1Sjk
Tlx3tm1Sjk/Tlx3tm1Sjk
involves: 129S2/SvPas * 129X1/SvJ MGI:3807393


Genotype
MGI:2668994
hm1
Allelic
Composition
Tlx1tm1Sjk/Tlx1tm1Sjk
Genetic
Background
involves: 129S2/SvPas
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tlx1tm1Sjk mutation (3 available); any Tlx1 mutation (20 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• many erythrocytes contain nuclear fragments of condensed DNA known as Howell-Jolly bodies, commonly associated with asplenia
• however, complete blood counts indicate that the number of red blood cells is normal
• homozygotes display a ~2-fold increase in the number of white blood cells relative to wild-type mice
• however, the B-cell and T-cell profile is normal in thymus, lymph node and peripheral blood
• in peripheral blood smears
• in peripheral blood smears
• at E12.5, mutant embryos display no cellular organization or mesenchymal cell condensation at the site of splenic development
• at E13.5, mutant embryos show no histological evidence of a splenic primordium within the dorsal mesogastrium
• at E12.5, mutant embryos display no mesenchymal cell condensation at the site of splenic development, indicating a specific, localized defect in mesodermal cells destined to form the spleen
• all adult homozygotes appear externally normal but display complete absence of spleen
• in contrast, all other internal organs (including the stomach and pancreas) are normal in morphology and position

immune system
• homozygotes display a ~2-fold increase in the number of white blood cells relative to wild-type mice
• however, the B-cell and T-cell profile is normal in thymus, lymph node and peripheral blood
• in peripheral blood smears
• in peripheral blood smears
• at E12.5, mutant embryos display no cellular organization or mesenchymal cell condensation at the site of splenic development
• at E13.5, mutant embryos show no histological evidence of a splenic primordium within the dorsal mesogastrium
• at E12.5, mutant embryos display no mesenchymal cell condensation at the site of splenic development, indicating a specific, localized defect in mesodermal cells destined to form the spleen
• all adult homozygotes appear externally normal but display complete absence of spleen
• in contrast, all other internal organs (including the stomach and pancreas) are normal in morphology and position

embryo
N
• despite observed gene expression in the branchial region of wild-type mice, homozygotes display no detectable abnormalities in branchial arches

nervous system
N
• despite observed gene expression in the developing hindbrain and cranial ganglia of wild-type mice, homozygotes display no detectable abnormalities in the hindbrain, cranial ganglia or cranial motor nuclei




Genotype
MGI:3807393
cx2
Allelic
Composition
Tlx1tm1Sjk/Tlx1tm1Sjk
Tlx3tm1Sjk/Tlx3tm1Sjk
Genetic
Background
involves: 129S2/SvPas * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tlx1tm1Sjk mutation (3 available); any Tlx1 mutation (20 available)
Tlx3tm1Sjk mutation (0 available); any Tlx3 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• double homozygotes exhibit improper development of most relay somatic sensory neurons, including the spinal-trigeminal nucleus, the dorsal horn of the spinal cord, and a portion of the principle trigeminal nucleus, as indicated by the loss or reduction of expression of specific molecular markers, and by the failure of ingrowth of trkA+ afferents to the trigeminal nucleus and the dorsal horn of the spinal cord
• at E14.5, trkA+ nociceptive/thermoceptive sensory afferents from double homozygous mutant mice are able to reach the dorsal entry zone but fail to enter the dorsal horn, unlike wild-type trkA+ afferents which start forming collateral branches into the spinal cord
• at E18.5, the ingrowth of trkA+ afferents in the double mutant spinal cord is much shallower than the projections noted in wild-type embryos; a similar defect is observed in the ingrowth of cranial trkA+ afferents to the spinal-trigeminal nucleus
• in contrast, projection of a subset of trkA+ afferents to the deep laminae of the spinal cord appears normal
• also, neuronal migration of dorsal horn neurons appears unaffected, as suggested by similar BrdU pulse-chase labeling patterns in wild-type and double mutant embryos
• at E14.5, number of somatostatin expressing neurons in dorsal spinal cord is increased 5-fold compared to wild-type embryos; most of the increase in neurons is confined to intermediate and deep dorsal laminas
• double homozygotes exhibit improper formation of two classes of dorsal interneurons, D2 and D4, as indicated by loss of specific marker (Isl1 and Lmx1b) expression
• double homozygotes display defective medullary D4 interneuron formation, as indicated by expression loss of both Lmx1b and Phox2a in the lateral area; not observed in single Tlx3tm1Sjk homozygotes
• however, no enhanced cell death is detected in E11.5-E14.5 double mutant embryos, as shown by TUNEL analysis
• number of somatostatin expressing neurons is reduced 5-fold in dorsal spinal cord at E18.75 due to absence of somatostatin in dorsal horn





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last database update
03/19/2024
MGI 6.23
The Jackson Laboratory