Long-Term Habitat Fragmentation Is Associated With Reduced MHC IIB Diversity and Increased Infections in Amphibian Hosts

Autor(es)

Belasen, Anat M. ^[1] ; Bletz, Molly C. ^[2] ; Leite, Domingos da Silva ^[3] ; Toledo, Luis Felipe ^[4] ; James, Timothy Y. ^[1]

Afiliação do(s) autor(es)

^[1] Univ Michigan, Dept Ecol & Evolutionary Biol, Ann Arbor, MI 48109 - USA

^[2] Univ Massachusetts, Dept Biol, Boston, MA 02125 - USA

^[3] Univ Estadual Campinas, Inst Biol, Campinas, SP - Brazil

^[4] Univ Estadual Campinas, Lab Hist Nat Anfibios Brasileiros, Dept Biol Anim, Inst Biol, Campinas, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: FRONTIERS IN ECOLOGY AND EVOLUTION; v. 6, JAN 10 2019.
• Citações Web of Science: 0

Resumo

Habitat fragmentation and wildlife disease are two widespread drivers of biodiversity loss, yet few empirical studies have explored their interactions. In this study, we utilized a naturally fragmented island system to examine the impacts of fragmentation on genetic diversity and amphibian infection dynamics. We determined the impacts of fragmentation on genetic diversity at the immunity locus MHC IIB, a hypothesized predictor of disease susceptibility. Contrary to the expectation that MHC diversity would remain high due to balancing selection, island populations lost genetic diversity at this locus while simultaneously experiencing positive selection at MHC IIB. We then used Next-Generation Sequencing to identify a variety of potential eukaryotic parasites from amphibian skin swabs. Island populations exhibited higher potential parasite richness (proportion of eukaryotic microbe operational taxonomic units or OTUs from parasitic taxa) relative to mainland populations. MHC homozygotes hosted a lower diversity of potential parasites, and population-level MHC diversity was negatively associated with parasite richness. Our results show that genetic erosion can occur at the MHC IIB locus following fragmentation, which may contribute to increased susceptibility to parasites. (AU)

• Processo FAPESP: 16/25358-3 - O fungo quitrídio no Brasil: da sua origem às suas consequências
• Beneficiário: Luis Felipe de Toledo Ramos Pereira
• Linha de fomento: Auxílio à Pesquisa - Temático