B6.129S2-Tlx1^tm1Sjk/J

Stock number: 002771
Product name: Hox11-
Research areas: Developmental Biology Research, Immunology, Inflammation and Autoimmunity Research, Internal/Organ Research

Description

These Tlx1 knock-out mice lack a spleen. They are suitable for use in applications related to the study of the role of the spleen in hematopoiesis and immunity.

Detailed description

Mice homozygous for the Tlx1^tm1Sjk targeted mutation lack a spleen; however, all other internal organs are normal. Characteristics include: dominant hemimelia (spontaneous mutation in the mouse), asplenia and many other defects including polydactyly or oligodactyly of the hindlimbs, tibial hemimelia, and sometimes reduction of the femur and pubic element of the pelvic girdle. Pharyngeal and mastication muscles derived from the branchial arches are present and anatomically normal homozygotes have normal cranial ganglia morphology and position and normal cranial motor nuclei function. There are normal numbers of RBCs but increased numbers of WBCs, including neutrophils and lymphocytes. The B-cell and T-cell profile is normal in the thymus, lymph nodes and peripheral blood. Many erythrocytes have nuclear fragments (Howell-Jolly bodies).

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

Development

Exon one (of three) was disrupted by PGK neo in the targeting vector. D3 ES cells were used.

Allele

Symbol: Tlx1^tm1Sjk
Name: targeted mutation 1, Stanley J Korsmeyer
MGI accession ID: MGI:1857260
Generation method: Targeted
Attributes: Null/Knockout
Marker symbol: Tlx1
Marker name: T cell leukemia, homeobox 1
Chromosome: 19
Strain of origin: 129S2/SvPas
Molecular note: Exon 1 was disrupted by the insertion of a neomycin selection cassette into codon 53. Transcript was undetected by in situ hybridization of homozygous mutant mice.