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BS90 光滑双脐螺对曼氏血吸虫感染的易感性作为一个显性等位基因在一组多态性的单次跨膜蛋白基因簇中分离。

Susceptibility of BS90 Biomphalaria glabrata snails to infection by SmLE Schistosoma mansoni segregates as a dominant allele in a cluster of polymorphic genes for single-pass transmembrane proteins.

机构信息

Department of Integrative Biology, Oregon State University, Corvallis, Oregon, United States of America.

Host Parasite Interaction Program, Texas Biomedical Research Institute, San Antonio, Texas, United States of America.

出版信息

PLoS Negl Trop Dis. 2024 Sep 16;18(9):e0012474. doi: 10.1371/journal.pntd.0012474. eCollection 2024 Sep.

DOI:10.1371/journal.pntd.0012474
PMID:39283952
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11426442/
Abstract

The trematodes that cause schistosomiasis in humans require aquatic snails as intermediate hosts. Identifying the genes in snails at which allelic variation controls resistance to infection by schistosomes could lead to novel ways to break the cycle of transmission. We therefore mapped genetic variation within the BS90 population of Biomphalaria glabrata snails that controls their resistance to infection by the SmLE population of Schistosoma mansoni. A marker in the PTC2 genomic region strongly associates with variation in resistance. The S-haplotype, which confers increased susceptibility, appears to be almost completely dominant to the R-haplotype, which confers increased resistance. This result suggests a model in which the parasite must match a molecule on the host side to successfully infect. The genomic region surrounding our marker shows high structural and sequence variability between haplotypes. It is also highly enriched for genes that code for single-pass transmembrane (TM1) genes. Several of the TM1 genes present on the S-haplotype lack orthologs on the R-haplotype, which makes them intriguing candidate genes in a model of dominant susceptibility. These results add to a growing body of work that suggests TM1 genes, especially those in this exceptionally diverse genomic region, may play an important role in snail-schistosome compatibility polymorphisms.

摘要

导致人体血吸虫病的吸虫需要水生蜗牛作为中间宿主。鉴定出蜗牛中控制对血吸虫感染的等位基因变异的基因,可能会开辟打破传播周期的新途径。因此,我们对控制 BS90 种群的 B. glabrata 蜗牛对 SmLE 种群的曼氏血吸虫感染的抗性进行了基因变异作图。PTC2 基因组区域中的一个标记与抗性的变异强烈相关。赋予易感性增加的 S 单倍型似乎几乎完全显性于赋予抗性增加的 R 单倍型。这一结果表明寄生虫必须匹配宿主侧的分子才能成功感染的模型。围绕我们的标记的基因组区域在单倍型之间显示出高度的结构和序列变异性。它还富含编码单次跨膜 (TM1) 基因的基因。S 单倍型上存在的几个 TM1 基因在 R 单倍型上没有同源基因,这使得它们成为显性易感性模型中的有趣候选基因。这些结果增加了越来越多的工作,表明 TM1 基因,特别是在这个异常多样化的基因组区域中的 TM1 基因,可能在蜗牛-血吸虫相容性多态性中发挥重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e41c/11426442/000b560e29e5/pntd.0012474.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e41c/11426442/cf3a23f052d0/pntd.0012474.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e41c/11426442/30312892d375/pntd.0012474.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e41c/11426442/40ae40cbc6cd/pntd.0012474.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e41c/11426442/48532024bbdf/pntd.0012474.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e41c/11426442/000b560e29e5/pntd.0012474.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e41c/11426442/cf3a23f052d0/pntd.0012474.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e41c/11426442/30312892d375/pntd.0012474.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e41c/11426442/40ae40cbc6cd/pntd.0012474.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e41c/11426442/48532024bbdf/pntd.0012474.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e41c/11426442/000b560e29e5/pntd.0012474.g005.jpg

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