Shin Dongyoung, Behura Susanta K, Severson David W
Florida Medical Entomology Laboratory, Department of Entomology and Nematology, University of Florida, Vero Beach, FL 32962, USA.
Department of Biological Sciences, University of Notre Dame, Notre Dame, IN 46556, USA.
Insects. 2019 Jan 10;10(1):25. doi: 10.3390/insects10010025.
is an important mosquito vector of several arboviruses, including dengue, yellow fever, Zika, and Chikungunya, which cause significant human morbidity and mortality globally. In certain populations of this mosquito, a native meiotic drive system causes abnormal spermatogenesis that results in highly male-biased progenies from some matings. Although the basic genetics and cytogenetics of the drive mechanism were elucidated, very little is known on a transcriptome level about how the meiotic drive phenotype is expressed in individual males. To address this question, we conducted a whole-genome microarray expression study of testes from a meiotic-drive-carrying strain (T37) in comparison with testes from a non-drive-carrying strain (RED). Based on bioinformatics analyses of the microarray data, we identified 209 genes associated with the meiotic drive phenotype that were significantly differentially expressed between the two strains. -means cluster analysis revealed nine clusters, in which genes upregulated in T37 testes were assigned to five clusters and genes downregulated in T37 testes were assigned to four clusters. Our data further revealed that genes related to protein translation, phosphorylation, and binding, as well as to G-protein-coupled receptor (GPCR) and peptidase activities, are differentially upregulated in testes from males with the meiotic drive genotype. Based on pathway analysis of these differentially expressed genes, it was observed that the glycosylphosphatidylinositol (GPI)-anchor biosynthesis pathway may play a role in the meiotic drive system. Overall, this investigation enhances our understanding of whole-genome gene expression associated with the meiotic drive system in .
是几种虫媒病毒的重要蚊子传播媒介，包括登革热、黄热病、寨卡病毒和基孔肯雅病毒，这些病毒在全球范围内导致大量人类发病和死亡。在这种蚊子的某些种群中，一种天然的减数分裂驱动系统会导致异常精子发生，从而在一些交配中产生高度偏雄的后代。尽管已经阐明了驱动机制的基本遗传学和细胞遗传学，但在转录组水平上，关于减数分裂驱动表型在个体雄性中如何表达的了解却很少。为了解决这个问题，我们对携带减数分裂驱动的品系（T37）的睾丸与不携带驱动的品系（RED）的睾丸进行了全基因组微阵列表达研究。基于对微阵列数据的生物信息学分析，我们鉴定出209个与减数分裂驱动表型相关的基因，它们在两个品系之间存在显著差异表达。均值聚类分析揭示了九个聚类，其中在T37睾丸中上调的基因被分配到五个聚类中，而在T37睾丸中下调的基因被分配到四个聚类中。我们的数据进一步表明，与蛋白质翻译、磷酸化和结合以及G蛋白偶联受体（GPCR）和肽酶活性相关的基因在具有减数分裂驱动基因型的雄性睾丸中差异上调。基于对这些差异表达基因的通路分析，观察到糖基磷脂酰肌醇（GPI）锚定生物合成通路可能在减数分裂驱动系统中发挥作用。总体而言，这项研究增强了我们对与减数分裂驱动系统相关的全基因组基因表达的理解。
