scholarly journals Extensive variation in the intelectin gene family in laboratory and wild mouse strains

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Faisal Almalki ◽  
Eric B. Nonnecke ◽  
Patricia A. Castillo ◽  
Alex Bevin-Holder ◽  
Kristian K. Ullrich ◽  
...  
Keyword(s):  
Mus Musculus ◽  
Wild Mouse ◽  
Large Deletion ◽  
Mouse Strains ◽  
Mus Musculus Domesticus ◽  
Wild Mice ◽  
Functional Studies ◽  
Full Complement ◽  
Mouse Species

AbstractIntelectins are a family of multimeric secreted proteins that bind microbe-specific glycans. Both genetic and functional studies have suggested that intelectins have an important role in innate immunity and are involved in the etiology of various human diseases, including inflammatory bowel disease. Experiments investigating the role of intelectins in human disease using mouse models are limited by the fact that there is not a clear one-to-one relationship between intelectin genes in humans and mice, and that the number of intelectin genes varies between different mouse strains. In this study we show by gene sequence and gene expression analysis that human intelectin-1 (ITLN1) has multiple orthologues in mice, including a functional homologue Itln1; however, human intelectin-2 has no such orthologue or homologue. We confirm that all sub-strains of the C57 mouse strain have a large deletion resulting in retention of only one intelectin gene, Itln1. The majority of laboratory strains have a full complement of six intelectin genes, except CAST, SPRET, SKIVE, MOLF and PANCEVO strains, which are derived from different mouse species/subspecies and encode different complements of intelectin genes. In wild mice, intelectin deletions are polymorphic in Mus musculus castaneus and Mus musculus domesticus. Further sequence analysis shows that Itln3 and Itln5 are polymorphic pseudogenes due to premature truncating mutations, and that mouse Itln1 has undergone recent adaptive evolution. Taken together, our study shows extensive diversity in intelectin genes in both laboratory and wild-mice, suggesting a pattern of birth-and-death evolution. In addition, our data provide a foundation for further experimental investigation of the role of intelectins in disease.

scholarly journals Extensive variation in the mouse intelectin gene family: recent duplications, deletions and inactivating variants result in diversity in laboratory strains

2021 ◽  
Author(s):  
Faisal Almalki ◽  
Eric B. Nonnecke ◽  
Patricia A. Castillo ◽  
Alex Bevin-Holder ◽  
Kristian K. Ullrich ◽  
...  
Keyword(s):  
Mus Musculus ◽  
Large Deletion ◽  
Mouse Strains ◽  
Mus Musculus Domesticus ◽  
Wild Mice ◽  
Functional Studies ◽  
Full Complement ◽  
Mouse Species ◽  
Inflammatory Bowel

AbstractIntelectins are a family of multimeric secreted proteins that bind microbe-specific glycans. Both genetic and functional studies have suggested that intelectins have an important role in innate immunity and are involved in the etiology of various human diseases, including inflammatory bowel disease. Experiments investigating the role of intelectins in human disease using mouse models are limited by the fact that there is not a clear one-to-one relationship between intelectin genes in humans and mice, and that the number of intelectin genes varies between different mouse strains. In this study we show by gene sequence and gene expression analysis that human intelectin-1 (ITLN1) has multiple orthologues in mice, including a functional homologue Itln1; however, human intelectin-2 has no such orthologue or homologue. We confirm that all sub-strains of the C57-line have a large deletion resulting in retention of only one intelectin gene, Itln1. The majority of laboratory strains have a full complement of six intelectin genes, except wild-derived CAST, SPRET, SKIVE, MOLF and PANCEVO, which are derived from different mouse species/subspecies and encode different complements of intelectin genes. In wild mice, intelectin deletions are polymorphic in Mus musculus castaneus and Mus musculus domesticus. Further sequence analysis shows that Itln3 and Itln5 are polymorphic pseudogenes due to premature truncating mutations, and that mouse Itln1 has undergone recent adaptive evolution. Taken together, our study shows extensive diversity in intelectin genes in both laboratory and wild-mice, suggesting a pattern of birth-and-death evolution. In addition, our data provide a foundation for further experimental investigation of the role of intelectins in disease.

Homology of p53 intronic sequences between four laboratory mouse strains and Japanese wild mouse (Mus musculus molossinus Mishima)

Genome ◽  
1994 ◽  
Vol 37 (6) ◽  
pp. 1022-1026 ◽  
Author(s):  
Masayuki Tokumitsu ◽  
Katsuhiro Ogawa
Keyword(s):  
Loss Of Heterozygosity ◽  
Mus Musculus ◽  
Laboratory Mouse ◽  
Wild Mouse ◽  
P53 Gene ◽  
Inbred Strains ◽  
Mouse Strains ◽  
Restriction Enzyme Digestion ◽  
Laboratory Mice ◽  
Wild Mice

Strain variation in the mouse p53 gene sequences was investigated in various regions of the gene in 14 inbred strains of laboratory mice and one Japanese wild mouse strain (Mus musculus molossinus Mishima, M. MOL-MSM). Nucleotides within p53 introns 1 and 7, found to be identical in 10 of the laboratory strains (129/J, A/J, AKR/J, BALB/cJ, C3H/HeJ, C57BL/6J, CBA/J, CE/J, NZB, and SWR/J), were substituted for other nucleotide sequences in common with M. MOL-MSM and the four other strains (DBA/1J, DBA/2J, I/LnJ, and P/J). The latter were documented to have originated from a common ancestor. These observations thus suggested the possibility that the p53 gene may have become substituted by outcrossing of this ancestral strain with Asian mice; this is presumably related to the documentation that Japanese mice brought to western countries were used as laboratory mice early in this century. To establish p53 gene heterozygosity, female C3H/HeJ and male DBA/2J mice were mated to produce F1, hybrids (C3D2F1,). Electrophoresis of PCR fragments including polymorphic regions with or without restriction enzyme digestion, allowed clear distinction of paternal and maternal p53 alleles. These markers, therefore, should be useful for studying the loss of heterozygosity of the p53 gene during the carcinogenic process.Key words: p53 gene, polymorphism, Japanese wild mice, laboratory mice, loss of heterozygosity.

scholarly journals Esterase alleles of inbred mouse strains maintained in The Netherlands

1988 ◽  
Vol 51 (1) ◽  
pp. 29-40 ◽  
Author(s):  
J. Hilgers ◽  
O. von Deimling ◽  
L. F. M. van Zutphen ◽  
R. ten Berg ◽  
R. Anand ◽  
...  
Keyword(s):  
Mus Musculus ◽  
Inbred Mouse ◽  
Chromosome 8 ◽  
Mouse Strains ◽  
Inbred Mouse Strains ◽  
Laboratory Mice ◽  
Mus Musculus Domesticus ◽  
Chinese Origin ◽  
Esterase Loci ◽  
Quantitative Manner

SummaryFifty-seven mouse strains were examined for genetic variation at 21 esterase loci. Three new alleles were found: Es-6d in strain A/WySna, Es-lle in FTC/CpbU and Es-18c in two WLL/BrA sublines. At most loci there was a single allele found in over 80% of strains, with one or two rare alleles. However, the Es-1, 3, 10, 13, 25 and 27 loci were much more polymorphic. Although several loci were linked on chomosomes 3, 8 and 9, linkage disequilibrium was only found between Es-5 and Es-11 (chromosome 8) and Es-26 and Es-27 (chromosome 3). There was also significant disequilibrium between Es-1 and 3, Es-1 and 10, and Es-3 and 10, which are on different chromosomes, suggesting that the 57 strains are not a random sample of inbred mouse strains. Fifty-four strains were closely related, with the Es-7b, –17a, –18a, –23c set of alleles, which are typical of Mus musculus domesticus. The three exceptional strains were MOL3 (Mus musculus molossinus), WLL/BrA (English–Norwegian origin) and TA2 (Chinese origin). There were 10 groups of strains which were identical at all loci. Sublines of the same strain were usually identical. Sometimes more distantly related strains, such as CBA/Bi, C3H/He, SM and DBA/Li, were identical, and in a few cases strains with no known common ancestry such as C58 and MAS were identical. Attempts to discriminate between a subset of 22 American and 15 European strains were unsuccessful, suggesting that the European strains add only in a quantitative manner to the gene pool of ‘laboratory mice’, whereas wild-derived strains such as MOL3 are genetically quite distinct from other laboratory mice.

scholarly journals Virological Properties and Nucleotide Sequences of Cas-E-Type Endogenous Ecotropic Murine Leukemia Viruses in South Asian Wild Mice, Mus musculus castaneus

2001 ◽  
Vol 75 (11) ◽  
pp. 5049-5058 ◽  
Author(s):  
Hidetoshi Ikeda ◽  
Kanako Kato ◽  
Hiroshi Kitani ◽  
Takako Suzuki ◽  
Takamasa Yoshida ◽  
...  
Keyword(s):  
Mus Musculus ◽  
Antigenic Variation ◽  
Wild Mouse ◽  
Wild Mice ◽  
Multiple Copies ◽  
Restricted Region ◽  
Genomic Dnas ◽  
Spontaneous Expression ◽  
Leukemia Viruses ◽  
Murine Leukemia

ABSTRACT Two types of endogenous ecotropic murine leukemia viruses (MuLVs), termed AKV- and Cas-E-type MuLVs, differ in nucleotide sequence and distribution in wild mouse subspecies. In contrast to AKV-type MuLV, Cas-E-type MuLV is not carried by common laboratory mice. Wild mice ofMus musculus (M. m.) castaneus carry multiple copies of Cas-E-type endogenous MuLV, including the Fv-4r gene that is a truncated form of integrated MuLV and functions as a host's resistance gene against ecotropic MuLV infection. Our genetic cross experiments showed that only the Fv-4r gene was associated with resistance to ecotropic F-MuLV infection. Because the spontaneous expression of infectious virus was not detected in M. m. castaneus, we generated mice that did not carry the Fv-4r gene but did carry a single or a few endogenous MuLV loci. In mice not carrying theFv-4r gene, infectious MuLVs were isolated in association with three of six Cas-E-type endogenous MuLV loci. The isolated viruses showed a weak syncytium-forming activity for XC cells, an interfering property of ecotropic MuLV, and a slight antigenic variation. Two genomic DNAs containing endogenous Cas-E-type MuLV were cloned and partially sequenced. All of the Cas-E-type endogenous MuLVs were closely related, hybrid-type viruses with an ecotropicenv gene and a xenotropic long terminal repeat. Duplications and a deletion were found in a restricted region of the hypervariable proline-rich region of Env glycoprotein.

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