共查询到20条相似文献,搜索用时 15 毫秒
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Derek P. Manzello Mikhail V. Matz Ian C. Enochs Lauren Valentino Renee D. Carlton Graham Kolodziej Xaymara Serrano Erica K. Towle Mike Jankulak 《Global Change Biology》2019,25(3):1016-1031
Identifying which factors lead to coral bleaching resistance is a priority given the global decline of coral reefs with ocean warming. During the second year of back‐to‐back bleaching events in the Florida Keys in 2014 and 2015, we characterized key environmental and biological factors associated with bleaching resilience in the threatened reef‐building coral Orbicella faveolata. Ten reefs (five inshore, five offshore, 179 corals total) were sampled during bleaching (September 2015) and recovery (May 2016). Corals were genotyped with 2bRAD and profiled for algal symbiont abundance and type. O. faveolata at the inshore sites, despite higher temperatures, demonstrated significantly higher bleaching resistance and better recovery compared to offshore. The thermotolerant Durusdinium trenchii (formerly Symbiondinium trenchii) was the dominant endosymbiont type region‐wide during initial (78.0% of corals sampled) and final (77.2%) sampling; >90% of the nonbleached corals were dominated by D. trenchii. 2bRAD host genotyping found no genetic structure among reefs, but inshore sites showed a high level of clonality. While none of the measured environmental parameters were correlated with bleaching, 71% of variation in bleaching resistance and 73% of variation in the proportion of D. trenchii was attributable to differences between genets, highlighting the leading role of genetics in shaping natural bleaching patterns. Notably, D. trenchii was rarely dominant in O. faveolata from the Florida Keys in previous studies, even during bleaching. The region‐wide high abundance of D. trenchii was likely driven by repeated bleaching associated with the two warmest years on record for the Florida Keys (2014 and 2015). On inshore reefs in the Upper Florida Keys, O. faveolata was most abundant, had the highest bleaching resistance, and contained the most corals dominated by D. trenchii, illustrating a causal link between heat tolerance and ecosystem resilience with global change. 相似文献
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Over the last 40 years, disease outbreaks have significantly reduced coral populations throughout the Caribbean. Most coral‐disease models assume that coral diseases are contagious and that pathogens are transmitted from infected to susceptible hosts. However, this assumption has not been rigorously tested. We used spatial epidemiology to examine disease clustering, at scales ranging from meters to tens of kilometers, to determine whether three of the most common Caribbean coral diseases, (i) yellow‐band disease, (ii) dark‐spot syndrome, and (iii) white‐plague disease, were spatially clustered. For all three diseases, we found no consistent evidence of disease clustering and, therefore, these diseases did not follow a contagious‐disease model. We suggest that the expression of some coral diseases is instead a two‐step process. First, environmental thresholds are exceeded. Second, these environmental conditions either weaken the corals, which are then more susceptible to infection, or the conditions increase the virulence or abundance of pathogens. Exceeding such environmental thresholds will most likely become increasingly common in rapidly warming oceans, leading to more frequent coral‐disease outbreaks. 相似文献
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Taylor C. Gibbons David C. H. Metzger Timothy M. Healy Patricia M. Schulte 《Molecular ecology》2017,26(10):2711-2725
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Pierre‐François Perroud Fabian B. Haas Manuel Hiss Kristian K. Ullrich Alessandro Alboresi Mojgan Amirebrahimi Kerrie Barry Roberto Bassi Sandrine Bonhomme Haodong Chen Juliet C. Coates Tomomichi Fujita Anouchka Guyon‐Debast Daniel Lang Junyan Lin Anna Lipzen Fabien Nogué Melvin J. Oliver Inés Ponce de León Ralph S. Quatrano Catherine Rameau Bernd Reiss Ralf Reski Mariana Ricca Younousse Saidi Ning Sun Péter Szövényi Avinash Sreedasyam Jane Grimwood Gary Stacey Jeremy Schmutz Stefan A. Rensing 《The Plant journal : for cell and molecular biology》2018,95(1):168-182
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Javier Terol Francisco Tadeo Daniel Ventimilla Manuel Talon 《Plant biotechnology journal》2016,14(3):938-950
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Huanan Zhang Feng Cheng Yuguo Xiao Xiaojun Kang Xiaowu Wang Rui Kuang Min Ni 《The Plant journal : for cell and molecular biology》2017,91(1):158-171
Seed development in dicots includes early endosperm proliferation followed by growth of the embryo to replace the endosperm. Endosperm proliferation in dicots not only provides nutrient supplies for subsequent embryo development but also enforces a space limitation, influencing final seed size. Overexpression of Arabidopsis SHORT HYPOCOTYL UNDER BLUE1::uidA (SHB1:uidA) in canola produces large seeds. We performed global analysis of the canola genes that were expressed and influenced by SHB1 during early endosperm proliferation at 8 days after pollination (DAP) and late embryo development at 13 DAP. Overexpression of SHB1 altered the expression of 973 genes at 8 DAP and 1035 genes at 13 DAP. We also surveyed the global SHB1 association sites, and merging of these sites with the RNA sequencing data identified a set of canola genes targeted by SHB1. The 8‐DAP list includes positive and negative genes that influence endosperm proliferation and are homologous to Arabidopsis MINI3, IKU2, SHB1, AGL62, FIE and AP2. We revealed a major role for SHB1 in canola endosperm development based on the dynamics of SHB1‐altered gene expression, the magnitude of SHB1 chromatin immunoprecipitation enrichment and the over‐representation of eight regulatory genes for endosperm development. Our studies focus on an important agronomic trait in a major crop for global agriculture. The datasets on stage‐specific and SHB1‐induced gene expression and genes targeted by SHB1 also provide a useful resource in the field of endosperm development and seed size engineering. Our practices in an allotetraploid species will impact similar studies in other crop species. 相似文献
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Robert Ekblom Paul Wennekes Gavin J. Horsburgh Terry Burke 《Molecular ecology resources》2014,14(3):636-646
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