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<p>The reed vole (<i>Microtus fortis</i>) serves as a significant rodent model, particularly distinguished by its robust natural resistance to <i>Schistosoma japonicum</i> infection. To unravel the genetic basis of this remarkable immunity, we present the first chromosome-level genome assembly for <i>M. fortis</i>. Employing PacBio HiFi long-read sequencing combined with Hi-C scaffolding, we constructed a high-quality 2.29&#xa0;Gb genome. This assembly is anchored into 26 pseudomolecules, achieving a contig N50 of 68.89&#xa0;Mb and incorporating 97.73% of the sequence into scaffolds. The genome demonstrates high completeness (BUSCO score 96.3%, glires_odb10) and a repeat content of 42.93%. Comparative genomic analysis revealed a high degree of synteny (95%) and a well-conserved chromosomal structure between <i>M. fortis</i> and <i>Mus musculus</i>.Phylogenetic analysis positions <i>M. fortis</i> diverging approximately 4.9 million years ago from other examined <i>Microtus</i> species and supports its classification within the <i>Alexandromys</i> subgenus. Notably, gene family evolution analysis identified significant expansions in immunity-related pathways. These expansions prominently involve T-cell receptor (TRAV, TRBV) and Major Histocompatibility Complex (MHC) class I and II genes. Further analysis highlighted an extensive lineage-specific expansion and diversification of the MHC class I gene family, predominantly clustered on chromosome 22. These genomic attributes, particularly the amplified T-cell receptor and MHC gene repertoires, are likely key contributors to the potent immune response and natural parasite resistance of <i>M. fortis</i>. This high-quality genome assembly provides an invaluable resource for advancing research into the adaptive evolution and unique biological traits of <i>M. fortis</i>, especially its parasite resistance mechanisms.</p>

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The Microtus fortis chromosome-level genome: illuminating adaptive evolution and natural parasite immunity

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年2月13日

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  • Du Zhang,
  • Qianwen Zhou,
  • Qi Hu,
  • Tianqiong He,
  • Jieling Xiao,
  • Junkang Zhou,
  • Yixin Wen,
  • Qian Liu,
  • Jing Zhang,
  • Wenlin Zhi,
  • Lingxuan Ouyang,
  • Suisui Gao,
  • Ruotong Guan,
  • Zhijun Zhou

摘要

The reed vole (Microtus fortis) serves as a significant rodent model, particularly distinguished by its robust natural resistance to Schistosoma japonicum infection. To unravel the genetic basis of this remarkable immunity, we present the first chromosome-level genome assembly for M. fortis. Employing PacBio HiFi long-read sequencing combined with Hi-C scaffolding, we constructed a high-quality 2.29 Gb genome. This assembly is anchored into 26 pseudomolecules, achieving a contig N50 of 68.89 Mb and incorporating 97.73% of the sequence into scaffolds. The genome demonstrates high completeness (BUSCO score 96.3%, glires_odb10) and a repeat content of 42.93%. Comparative genomic analysis revealed a high degree of synteny (95%) and a well-conserved chromosomal structure between M. fortis and Mus musculus.Phylogenetic analysis positions M. fortis diverging approximately 4.9 million years ago from other examined Microtus species and supports its classification within the Alexandromys subgenus. Notably, gene family evolution analysis identified significant expansions in immunity-related pathways. These expansions prominently involve T-cell receptor (TRAV, TRBV) and Major Histocompatibility Complex (MHC) class I and II genes. Further analysis highlighted an extensive lineage-specific expansion and diversification of the MHC class I gene family, predominantly clustered on chromosome 22. These genomic attributes, particularly the amplified T-cell receptor and MHC gene repertoires, are likely key contributors to the potent immune response and natural parasite resistance of M. fortis. This high-quality genome assembly provides an invaluable resource for advancing research into the adaptive evolution and unique biological traits of M. fortis, especially its parasite resistance mechanisms.