The geographic and biological diversity of China has resulted in the differential adaptation of the eastern honeybee, Apis cerana, to these varied habitats. A. cerana were collected from 14 locations in China. Their genomes were sequenced, and nucleotide polymorphisms were identified at more than 9 million sites. Both STRUCTURE and principal component analysis placed the bees into seven groups. Phylogenomic analysis groups the honeybees into many of the same clusters with high bootstrap values (91%–100%). Populations from Tibet and South Yunnan are sister taxa and together represent the earliest diverging lineage included in this study. We propose that the evolutionary origin of A. cerana in China was in the southern region of Yunnan Province and expanded from there into the southeastern regions and into the northeastern mountain regions. The Cold‐Temperate West Sichuan Plateau and Tropical Diannan populations were compared to identify genes under adaptive selection in these two habitats. Pathway enrichment analysis showing genes under selection, including the Hippo signaling pathway, GABAergic pathway, and trehalose‐phosphate synthase, indicates that most genes under selection pressure are involved in the process of signal transduction and energy metabolism. qRT‐PCR analysis reveals that one gene under selection, the AcVIAAT gene, involved in the GABAergic pathway, is responding to cold temperature stress. Through homologous recombination, we show that the AcVIAAT gene is able to replace the CNAG_01904 gene in the fungus Cryptococcus neoformans and that it makes the fungus less sensitive to conditions of oxidative stress and variations in temperature. Our results contribute to our understanding of the evolutionary origin of A. cerana in China and the molecular basis of environmental adaptation. 相似文献
Intracerebral hemorrhage (ICH) causes long term neurological abnormality or death. Oxidative stress is closely involved in ICH mediated brain damage. Steroid receptor cofactor 3 (SRC-3), a p160 family member, is widely expressed in the brain and regulates transactivation of Nrf2, a key component of antioxidant response. Our study aims to test if SRC-3 is implicated in ICH mediated brain injury. We first examined levels of SRC-3 and oxidative stress in the brain of mice following ICH and analyzed their correlation. Then ICH was induced in wild type (WT) and SRC-3 knock out mice and how SRC-3 deletion affected ICH induced brain damage, oxidative stress and behavioral outcome was assessed. We found that SRC-3 mRNA and protein expression levels were reduced gradually after ICH induction in WT mice along with an increase in oxidative stress levels. Correlation analysis revealed that SRC-3 mRNA levels negatively correlated with oxidative stress. Deletion of SRC-3 further increased ICH induced brain edema, neurological deficit score and oxidative stress and exacerbated ICH induced behavioral abnormality including motor dysfunction and cognitive impairment. Our findings suggest that SRC-3 is involved in ICH induced brain injury, probably through modulation of oxidative stress.