Plant pathogenic fungi represent the largest group of disease-causing agents on crop plants, and are a constant and major threat to agriculture worldwide. Recent studies have shown that engineered production of RNA interference (RNAi)-inducing dsRNA in host plants can trigger specific fungal gene silencing and confer resistance to fungal pathogens. Although these findings illustrate efficient uptake of host RNAi triggers by pathogenic fungi, it is unknown whether or not such an uptake mechanism has been evolved for a natural biological function in fungus-host interactions. Here, we show that in response to infection with Verticillium dahliae (a vascular fungal pathogen responsible for devastating wilt diseases in many crops) cotton plants increase production of microRNA 166 (miR166) and miR159 and export both to the fungal hyphae for specific silencing. We found that two V. dahliae genes encoding a Ca-dependent cysteine protease (Clp-1) and an isotrichodermin C-15 hydroxylase (HiC-15), and targeted by miR166 and miR159, respectively, are both essential for fungal virulence. Notably, V. dahliae strains expressing either Clp-1 or HiC-15 rendered resistant to the respective miRNA exhibited drastically enhanced virulence in cotton plants. Together, our findings identify a novel defence strategy of host plants by exporting specific miRNAs to induce cross-kingdom gene silencing in pathogenic fungi and confer disease resistance.

Rainbow trout (Oncorhynchus mykiss Walbaum) in southern Western Australia have undergone passive selection for over 19 generations to survive high water temperatures. Based on the conceptual model of 'oxygen-and capacity-limited thermal tolerance', we measured critical thermal maximum (CT max ), maximum heart rate ( f H,max ) and aerobic scope to test the hypothesis that these rainbow trout can maintain aerobic scope at high temperatures through a robust cardiac performance supporting oxygen delivery. Across five family groups CT max averaged 29.0±0.02°C. Aerobic scope was maximized at 15.8±0.3°C (T opt ), while the upper pejus temperature (T pej , set at 90% of maximum aerobic scope) was 19.9±0.3°C. Although aerobic scope decreased at temperatures above T opt , the value at 25°C remained well over 40% of the maximum. Furthermore, pharmacologically stimulated f H,max increased with temperature, reaching a peak value between 23.5±0.4 and 24.0±0.4°C (T max ) for three family groups. The Arrhenius breakpoint temperature (T AB ) for f H,max was 20.3±0.3 to 20.7±0.4°C, while the average Q 10 breakpoint temperature (T QB , when the incremental Q 10 <1.6) for f H,max was 21.6±0.2 to 22.0±0.4°C. Collectively, f H,max progressively became less temperature dependent beyond 20°C (T AB and T QB ), which coincides with the upper T pej for aerobic scope. Although upper thermal performance indices for both aerobic scope and f H,max were compared among family groups in this population, appreciable differences were not evident. Compared with other populations of rainbow trout, the present assessment is consistent with the prediction that this strain has undergone selection and shows the ability to tolerate higher water temperatures.

Heterogeneous and ever-changing thermal environments drive the evolution of populations and species, especially when extreme conditions increase selection pressure for traits influencing fitness. However, projections of biological diversity under scenarios of climate change rarely consider evolutionary adaptive potential of natural species. In this study, we tested for mechanistic evidence of evolutionary thermal adaptation among ecologically divergent redband trout populations (Oncorhynchus mykiss gairdneri) in cardiorespiratory function, cellular response and genomic variation. In a common garden environment, fish from an extreme desert climate had significantly higher critical thermal maximum (p < .05) and broader optimum thermal window for aerobic scope (>3°C) than fish from cooler montane climate. In addition, the desert population had the highest maximum heart rate during warming (20% greater than montane populations), indicating improved capacity to deliver oxygen to internal tissues. In response to acute heat stress, distinct sets of cardiac genes were induced among ecotypes, which helps to explain the differences in cardiorespiratory function. Candidate genomic markers and genes underlying these physiological adaptations were also pinpointed, such as genes involved in stress response and metabolic activity (hsp40, ldh-b and camkk2). These markers were developed into a multivariate model that not only accurately predicted critical thermal maxima, but also evolutionary limit of thermal adaptation in these specific redband trout populations relative to the expected limit for the species. This study demonstrates mechanisms and limitations of an aquatic species to evolve under changing environments that can be incorporated into advanced models to predict ecological consequences of climate change for natural organisms.

Temperature is a master environmental factor that limits the geographical distribution of species, especially in ectotherms. To address challenges in biodiversity conservation under ongoing climate change, it is essential to characterize relevant functional limitations and adaptive genomic content at population and species levels. Here, we present evidence for adaptive divergence in cardiac function and genomic regions in redband trout (Oncorhynchus mykiss gairdneri) populations from desert and montane streams. Cardiac phenotypes of individual fish were measured in the field with a custom‐built electrocardiogram apparatus. Maximum heart rate and its rate limiting temperature during acute warming were significantly higher in fish that have evolved in the extreme of a desert climate compared to a montane climate. Association mapping with 526,301 single nucleotide polymorphisms (SNPs) across the genome revealed signatures of thermal selection both within and among ecotypes. Among desert and montane populations, 435 SNPs were identified as putative outliers under natural selection and 20 of these loci showed significant association with average summer water temperatures among populations. Phenotypes for cardiac performance were variable within each ecotype, and 207 genomic regions were strongly associated with either maximum heart rate or rate limiting temperatures among individuals. Annotation of significant loci provided candidate genes that underlie thermal adaptation, including pathways associated with cardiac function (IRX5, CASQ1, CAC1D, and TITIN), neuroendocrine system (GPR17 and NOS), and stress response (SERPH). By integrating comparative physiology and population genomics, results here advance our knowledge on evolutionary processes of thermal adaptation in aquatic ectotherms.

With global temperatures projected to surpass the limits of thermal tolerance for many species, evaluating the heritable variation underlying thermal tolerance is critical for understanding the potential for adaptation to climate change. We examined the evolutionary potential of thermal tolerance within a population of chinook salmon (Oncorhynchus tshawytscha) by conducting a full-factorial breeding design and measuring the thermal performance of cardiac function and the critical thermal maximum (CT max ) of offspring from each family. Additive genetic variation in offspring phenotype was mostly negligible, although these direct genetic effects explained 53% of the variation in resting heart rate ( f H ). Conversely, maternal effects had a significant influence on resting f H , scope for f H , cardiac arrhythmia temperature and CT max . These maternal effects were associated with egg size, as indicated by strong relationships between the mean egg diameter of mothers and offspring thermal tolerance. Because egg size can be highly heritable in chinook salmon, our finding indicates that the maternal effects of egg size constitute an indirect genetic effect contributing to thermal tolerance. Such indirect genetic effects could accelerate evolutionary responses to the selection imposed by rising temperatures and could contribute to the population-specific thermal tolerance that has recently been uncovered among Pacific salmon populations.

Epithelial-mesenchymal transition (EMT) is essential in asthma airway remodeling. IL-33 from epithelial cells is involved in pulmonary fibrosis. CD146 has been extensively explored in cancer-associated EMT. Whether IL-33 regulates CD146 in the EMT process associated with asthma airway remodeling is still largely unknown. We hypothesized that EMT in airway remodeling was regulated by the IL-33/CD146 axis. House dust mite (HDM) extract increased the expression of IL-33 and CD146 in epithelial cells. Increased expression of CD146 in HDM-treated epithelial cells could be blocked with an ST2-neutralizing antibody. Moreover, HDM-induced EMT was dependent on the CD146 and TGF-β/SMAD-3 signaling pathways. IL-33 deficiency decreased CD146 expression and alleviated asthma severity. Similarly, CD146 deficiency mitigated EMT and airway remodeling in a murine model of chronic allergic airway inflammation. Furthermore, CD146 expression was significantly elevated in asthma patients. We concluded that IL-33 from HDM extract-treated alveolar epithelial cells stimulated CD146 expression, promoting EMT in airway remodeling in chronic allergic inflammation.

A goal of studying local adaptation is to identify the underlying genetic variation (i.e., genes and nucleotide polymorphisms) in natural populations. However, it is a challenging task since in most natural ecosystems, multiple environmental factors work together in complex ways to alter selection on a combination of traits and influence overall fitness. For example, water temperature has a pervasive effect on development, swimming performance, reproduction, and survival of ectothermic aquatic species (Beacham & Murray, 1989

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