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991.
McLachlan Rowan H. Price James T. Muñoz-Garcia Agustí Weisleder Noah L. Jury Christopher P. Toonen Robert J. Grottoli Andréa G. 《Coral reefs (Online)》2021,40(5):1505-1523
Coral Reefs - To evaluate potential coral adaptive mechanisms, we investigated physiological traits (biomass, lipid, protein, chlorophyll, and isotopic proxies for trophic strategy) in eight... 相似文献
992.
Maloyjo Joyraj Bhattacharjee Jinn-Jy Lin Chih-Yao Chang Yu-Ting Chiou Tian-Neng Li Chia-Wei Tai Tz-Fan Shiu Chi-An Chen Chia-Yi Chou Paromita Chakraborty Yan Yuan Tseng Lily Hui-Ching Wang Wen-Hsiung Li 《Molecular biology and evolution》2021,38(7):2715
SARS-CoV-2 infects humans through the binding of viral S-protein (spike protein) to human angiotensin I converting enzyme 2 (ACE2). The structure of the ACE2-S-protein complex has been deciphered and we focused on the 27 ACE2 residues that bind to S-protein. From human sequence databases, we identified nine ACE2 variants at ACE2–S-protein binding sites. We used both experimental assays and protein structure analysis to evaluate the effect of each variant on the binding affinity of ACE2 to S-protein. We found one variant causing complete binding disruption, two and three variants, respectively, strongly and mildly reducing the binding affinity, and two variants strongly enhancing the binding affinity. We then collected the ACE2 gene sequences from 57 nonhuman primates. Among the 6 apes and 20 Old World monkeys (OWMs) studied, we found no new variants. In contrast, all 11 New World monkeys (NWMs) studied share four variants each causing a strong reduction in binding affinity, the Philippine tarsier also possesses three such variants, and 18 of the 19 prosimian species studied share one variant causing a strong reduction in binding affinity. Moreover, one OWM and three prosimian variants increased binding affinity by >50%. Based on these findings, we proposed that the common ancestor of primates was strongly resistant to and that of NWMs was completely resistant to SARS-CoV-2 and so is the Philippine tarsier, whereas apes and OWMs, like most humans, are susceptible. This study increases our understanding of the differences in susceptibility to SARS-CoV-2 infection among primates. 相似文献
993.
Rhett M Rautsaw Tristan D Schramer Rachel Acua Lindsay N Arick Mark DiMeo Kathryn P Mercier Michael Schrum Andrew J Mason Mark J Margres Jason L Strickland Christopher L Parkinson 《Molecular biology and evolution》2021,38(3):745
The migration-selection balance often governs the evolution of lineages, and speciation with gene flow is now considered common across the tree of life. Ecological speciation is a process that can facilitate divergence despite gene flow due to strong selective pressures caused by ecological differences; however, the exact traits under selection are often unknown. The transition from freshwater to saltwater habitats provides strong selection targeting traits with osmoregulatory function. Several lineages of North American watersnakes (Nerodia spp.) are known to occur in saltwater habitat and represent a useful system for studying speciation by providing an opportunity to investigate gene flow and evaluate how species boundaries are maintained or degraded. We use double digest restriction-site associated DNA sequencing to characterize the migration-selection balance and test for evidence of ecological divergence within the Nerodia fasciata-clarkii complex in Florida. We find evidence of high intraspecific gene flow with a pattern of isolation-by-distance underlying subspecific lineages. However, we identify genetic structure indicative of reduced gene flow between inland and coastal lineages suggesting divergence due to isolation-by-environment. This pattern is consistent with observed environmental differences where the amount of admixture decreases with increased salinity. Furthermore, we identify significantly enriched terms related to osmoregulatory function among a set of candidate loci, including several genes that have been previously implicated in adaptation to salinity stress. Collectively, our results demonstrate that ecological differences, likely driven by salinity, cause strong divergent selection which promotes divergence in the N. fasciata-clarkii complex despite significant gene flow. 相似文献
994.
Yan Yan Zhao Sihan Ding Zehong Tie Weiwei Hu Wei 《Plant Molecular Biology Reporter》2021,39(3):607-616
Plant Molecular Biology Reporter - Cassava is an important starchy and food crop; however, the commercial value of cassava is seriously constrained by postharvest physiological deterioration (PPD).... 相似文献
995.
Huang Lihong Fu Qiang Dai Jia-Meng Yan Bing-Chao Wang Dawei Puno Pema-Tenzin Yue Jianbo 《Cell biology and toxicology》2021,37(5):695-713
Cell Biology and Toxicology - Autophagy is a conserved lysosomal degradation process, and abnormal autophagy has been associated with various pathological processes, e.g., neurodegeneration,... 相似文献
996.
Daisylyn Senna Tan Yanpu Chen Ya Gao Anastasia Bednarz Yuanjie Wei Vikas Malik Derek Hoi-Hang Ho Mingxi Weng Sik Yin Ho Yogesh Srivastava Sergiy Velychko Xiaoxiao Yang Ligang Fan Johnny Kim Johannes Graumann Gary D. Stormo Thomas Braun Jian Yan Hans R. Schler Ralf Jauch 《Molecular biology and evolution》2021,38(7):2854
997.
998.
Our current research aimed to decipher the role and underlying mechanism with regard to miR-29b-3p involving in myocardial ischemia/reperfusion (I/R) injury. In the present study, cardiomyocyte H9c2 cell was used, and hypoxia/reoxygenation (H/R) model was established to mimic the myocardial I/R injury. The expressions of miR-29b-3p and pentraxin 3 (PTX3) were quantified deploying qRT-PCR and Western blot, respectively. The levels of LDH, TNF-α, IL-1β and IL-6 were detected to evaluate cardiomyocyte apoptosis and inflammatory response. Cardiomyocyte viability and apoptosis were examined employing CCK-8 assay and flow cytometry, respectively. Verification of the targeting relationship between miR-29b-3p and PTX3 was conducted using a dual-luciferase reporter gene assay. It was found that miR-29b-3p expression in H9c2 cells was up-regulated by H/R, and a remarkable down-regulation of PTX3 expression was demonstrated. MiR-29b-3p significantly promoted of release of inflammatory cytokines of H9c2 cells, and it also constrained the proliferation and promoted the apoptosis of H9c2 cells. Additionally, PTX3 was inhibited by miR-29b-3p at both mRNA and protein levels, and it was identified as a direct target of miR-29b-3p. PTX3 overexpression could reduce the inflammatory response, increase the viability of H9c2 cells, and inhibit apoptosis. Additionally, PTX3 counteracted the function of miR-29b-3p during the injury of H9c2 cells induced by H/R. In summary, miR-29b-3p was capable of aggravating the H/R injury of H9c2 cells by repressing the expression of PTX3. 相似文献
999.
Mayarling Francisca Troncoso Jafet Ortiz-Quintero Valeria Garrido-Moreno Fernanda Sanhueza-Olivares Alejandra Guerrero-Moncayo Mario Chiong Pablo F. Castro Lorena García Luigi Gabrielli Ramón Corbalán Luis Garrido-Olivares Sergio Lavandero 《生物化学与生物物理学报:疾病的分子基础》2021,1867(9):166170
The vascular cellular adhesion molecule-1 (VCAM-1) is a protein that canonically participates in the adhesion and transmigration of leukocytes to the interstitium during inflammation. VCAM-1 expression, together with soluble VCAM-1 (sVCAM-1) induced by the shedding of VCAM-1 by metalloproteinases, have been proposed as biomarkers in immunological diseases, cancer, autoimmune myocarditis, and as predictors of mortality and morbidity in patients with chronic heart failure (HF), endothelial injury in patients with coronary artery disease, and arrhythmias. This revision aims to discuss the role of sVCAM-1 as a biomarker to predict the occurrence, development, and preservation of cardiovascular disease. 相似文献
1000.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with unclear pathogenesis. We previously reported that syngenetic, activated lymphocyte-derived DNA (ALD-DNA) could robustly elicit macrophage activation, which plays an important role in the pathogenesis of murine lupus nephritis. In addition, extracellular HMGB1 obviously facilitated the accumulation of ALD-DNA in endosomes and promoted macrophage inflammation. While the detailed mechanism was still unknown. In this study, we found that HMGB1 could obviously change the DNA uptake pathways in macrophages. ALD-DNA alone was mainly uptake by the low efficient and unselective macropinocytosis, while extracellular HMGB1 potently promoted the more efficient and specific clathrin-/caveolin-1-dependent receptor-mediated endocytosis pathways, and led to the rapid and abundant aggregation of ALD-DNA in endosomes. This effect relied on the DNA binding ability and TLR2/TLR4 of HMGB1. Our study not only helped us to understand the promotion mechanisms of extracellular HMGB1 on ALD-DNA-induced macrophage inflammation, but also provided some clues to the pathogenesis of SLE. 相似文献