Calpain 11 is unique to mouse spermatogenic cells

The calpains are a family of calcium-dependent thiol proteases involved in intracellular processing of proteins. They occur as heterodimers containing one of various large subunits and a common small subunit. Some of the large subunits are expressed ubiquitously and others are expressed in a restricted set of tissues. We have cloned the cDNA for mouse calpain 11 and demonstrated that it is expressed specifically in the mouse testis. The mRNA begins to accumulate in the testis between days 14 and 16 after birth, corresponding to the period of pachytene spermatocyte development. The protein is detected by day 18 after birth, during mid to late pachytene spermatocyte development, and is present in the acrosomal region of spermatozoa from the cauda epididymis. The expression of calpain 11 during spermatogenesis and its localization in spermatozoa suggest that it is involved in regulating calcium-dependent signal transduction events during meiosis and sperm functional processes.     

Susceptibility to streptozotocin-induced diabetes is mapped to mouse chromosome 11

To study the contribution of beta-cell vulnerability to susceptibility to diabetes, we studied beta-cell vulnerability to a single high dose of streptozotocin (STZ) in an animal model of type 2 diabetes, the NSY mouse, a sister strain of the STZ-sensitive NOD mouse, in comparison with the STZ-resistant C3H mouse. NSY mice were found to be extremely sensitive to STZ. Introgression of a single Chr 11, where STZ-sensitivity was mapped in the NOD mouse, from NSY mice converted STZ-resistant C3H mice to STZ-sensitive. Two nucleotide substitutions were identified in the nucleoredoxin gene, a positional and functional candidate gene for STZ-induced diabetes on Chr 11. These data, together with the co-localization of type 1 (Idd4) and type 2 (Nidd1n) susceptibility genes on Chr 11, suggest that the intrinsic vulnerability of pancreatic beta cells is determined by a gene or genes on Chr 11, which may also contribute to susceptibility to spontaneous diabetes.     

Genetic mapping of the mouse interleukin 3 gene to chromosome 11

Interleukin 3 (IL 3) is a T cell-derived lymphokine that induces the proliferation and differentiation of early hematopoietic stem cells. By using a cDNA clone for IL 3, a single Eco-RI restriction fragment of 8.5 kbp was detected in Southern blot hybridizations of DNA from BALB/c and C57BL/10 mice, whereas an Eco-RI restriction fragment of 10.8 kbp was detected in NFS and A/J mice. Under the conditions used, no hybridization was detected to Chinese hamster DNA. The species and strain differences were used to analyze a series of hamster X mouse somatic cell hybrids and genetic crosses between NFS and C57BL/10 mice. The results demonstrate that the IL 3 gene is located on chromosome 11.     

Genetic mapping of the mouse ferritin light chain gene and 11 pseudogenes on 11 mouse chromosomes

We typed the progeny of two sets of genetic crosses to determine the map locations for loci containing sequences related to the ferritin light chain (Ft11) gene. Twelve loci were positioned on 11 different chromosomes. One of these genes mapped to a position on Chr 7 predicted to contain the expressed gene on the basis of the previously determined position of the human homolog on 19q13.3-q13.4. Received: 23 July 1997 / Accepted: 20 September 1997     

Two new mouse chromosome 11 balancers

Segmental inversions causing recombination suppression are an essential feature of balancer chromosomes. Meiotic crossing over between homologous chromosomes within an inversion interval will lead to nonviable gametes, while gametes generated from recombination events elsewhere on the chromosome will be unaffected. This apparent recombination suppression has been widely exploited in genetic studies in Drosophila to maintain and analyze stocks carrying recessive lethal mutations. Balancers are particularly useful in mutagenesis screens since they help to establish the approximate genomic location of alleles of genes causing phenotypes. Using the Cre-loxP recombination system, we have constructed two mouse balancer chromosomes carrying 8- and 30-cM inversions between Wnt3 and D11Mit69 and between Trp53 and EgfR loci, respectively. The Wnt3-D11Mit69 inversion mutates the Wnt3 locus and is therefore homozygous lethal. The Trp53-EgfR inversion is homozygous viable, since the EgfR locus is intact and mutations in p53 are homozygous viable. A dominantly acting K14-agouti minigene tags both rearrangements, which enables these balancer chromosomes to be visibly tracked in mouse stocks. With the addition of these balancers to the previously reported Trp53-Wnt3 balancer, most of mouse chromosome 11 is now available in balancer stocks.     

Erbb is linked to the alpha-globin locus on mouse chromosome 11.

A fragment of the human gene for c-erb-B was used to map homologous sequences in mice. Analysis of somatic cell hybrids and recombinant inbred and congenic mouse strains indicated that this gene, designated Erbb, is closely linked to the gene for alpha-globin on mouse chromosome 11. Several genes controlling hematopoietic differentiation map to mouse chromosome 11.     

The major locus for multifactorial nonsyndromic cleft lip maps to mouse Chromosome 11

Cleft lip with or without cleft palate, CL(P), a common human birth defect, has a genetically complex etiology. An animal model with a similarly complex genetic basis is established in the A/WySn mouse strain, in which 20% of newborn have CL(P). Using a newly created congenic strain, AEJ.A, and SSLP markers, we have mapped a major CL(P)-causing gene derived from the A/WySn strain. This locus, here named clf1 (cleft lip) maps to Chromosome (Chr) 11 to a region having linkage homology with human 17q21-24, supporting reports of association of human CL(P) with the retinoic acid receptor alpha (RARA) locus.     

Localization of the mouse thymidine kinase gene to the distal portion of chromosome 11

We report the cytogenetic mapping of the thymidine kinase (tk-1) gene in the mouse using two complementary and independent analyses: (1) investigation of chromosome aberrations associated with tk-1 gene inactivation in the L5178Y TK+/- -3.7.2C cell line, and (2) fluorescence in situ molecular hybridization of cloned tk-1 cDNA probes to mitotic chromosomes of this cell line. The consensus location from both analyses is 11E1-E2. Consideration of the mouse tk-1 gene localization, along with evidence that the homologous human TK1 gene is located distally on the large arm of chromosome 17, appears to extend the region of homology between MMU11 and HSA17 to the distal end of both chromosomes.     

Localization of the growth hormone gene to the distal half of mouse chromosome 11

A DNA fragment size variant for the growth hormone gene, Gh, has been identified among inbred strains of mice. The inbred strains SM/J and CAST/Ei carry the less frequent allele Ghb and 11 other strains carry the Gha allele. Segregation analysis of data from two crosses involving SM/J and NZB/BINJ and a cross involving BALB/cJ and CAST/Ei confirmed the assignment of Gh to mouse chromosome 11 and placed the locus 2.6 +/- 1.8 map units distal to Erba (avian erythroblastosis oncogene A), a position consistent with the assignment of the Gh locus to the q22-q24 region of chromosome 17 on the human map. Segregation analysis also refined the location of Sparc (secreted acidic cysteine-rich glycoprotein) on mouse chromosome 11 to a position 16.7 +/- 4.2 map units proximal to Evi-2 (ecotropic viral integration site 2).