Extensive variation in the intelectin gene family in laboratory and wild mouse strains.
Extensive variation in the intelectin gene family in laboratory and wild mouse strains.
复制标题
在实验室和野鼠品系中intelectin基因家族的广泛变异。
DOI:
10.1038/s41598-021-94679-3
复制
发表时间:
2021-07-30
影响因子:
4.6
通讯作者:
Hollox EJ
中科院分区:
文献类型:
--
作者:
Almalki F;Nonnecke EB;Castillo PA;Bevin-Holder A;Ullrich KK;Lönnerdal B;Odenthal-Hesse L;Bevins CL;Hollox EJ
Intelectins 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.
登录
查看更多内容
影响因子:
30.8
作者:
通讯作者:
--
影响因子:
9.8
作者:
Harr, Bettina;Karakoc, Emre;Neme, Rafik;Teschke, Meike;Pfeifle, Christine;Pezer, Zeljka;Babiker, Hiba;Linnenbrink, Miriam;Montero, Inka;Scavetta, Rick;Abai, Mohammad Reza;Puente Molins, Marta;Schlegel, Mathias;Ulrich, Rainer G.;Altmueller, Janine;Franitza, Marek;Buentge, Anna;Kuenzel, Sven;Tautz, Diethard
通讯作者:
Tautz, Diethard
影响因子:
10.7
作者:
Kumar, Sudhir;Stecher, Glen;Tamura, Koichiro
通讯作者:
Tamura, Koichiro
DOI:
10.1093/bioinformatics/btp352
发表时间:
2009-08-15
期刊:
Bioinformatics (Oxford, England)
影响因子:
--
作者:
Li H;Handsaker B;Wysoker A;Fennell T;Ruan J;Homer N;Marth G;Abecasis G;Durbin R;1000 Genome Project Data Processing Subgroup
通讯作者:
1000 Genome Project Data Processing Subgroup
影响因子:
5.8
作者:
Danecek, Petr;Auton, Adam;Durbin, Richard
通讯作者:
Durbin, Richard