Excessive rainfall leads to maize yield loss of a comparable magnitude to extreme drought in the United States

Increasing drought and extreme rainfall are major threats to maize production in the United States. However, compared to drought impact, the impact of excessive rainfall on crop yield remains unresolved. Here, we present observational evidence from crop yield and insurance data that excessive rainfall can reduce maize yield up to ?34% (?17 ± 3% on average) in the United States relative to the expected yield from the long‐term trend, comparable to the up to ?37% loss by extreme drought (?32 ± 2% on average) from 1981 to 2016. Drought consistently decreases maize yield due to water deficiency and concurrent heat, with greater yield loss for rainfed maize in wetter areas. Excessive rainfall can have either negative or positive impact on crop yield, and its sign varies regionally. Excessive rainfall decreases maize yield significantly in cooler areas in conjunction with poorly drained soils, and such yield loss gets exacerbated under the condition of high preseason soil water storage. Current process‐based crop models cannot capture the yield loss from excessive rainfall and overestimate yield under wet conditions. Our results highlight the need for improved understanding and modeling of the excessive rainfall impact on crop yield.     

Splenic gene expression profiling in White Leghorn layer inoculated with the Salmonella enterica serovar Enteritidis

Salmonella enterica serovar Enteritidis (SE) is a foodborne pathogen that can threaten human health through contaminated poultry products. Live poultry, chicken eggs and meat are primary sources of human salmonellosis. To understand the genetic resistance of egg‐type chickens in response to SE inoculation, global gene expression in the spleen of 20‐week‐old White Leghorn was measured using the Agilent 4 × 44 K chicken microarray at 7 and 14 days following SE inoculation (dpi). Results showed that there were 1363 genes significantly differentially expressed between inoculated and non‐inoculated groups at 7 dpi (I7/N7), of which 682 were up‐regulated and 681 were down‐regulated genes. By contrast, 688 differentially expressed genes were observed at 14 dpi (I14/N14), of which 371 were up‐regulated genes and 317 were down‐regulated genes. There were 33 and 28 immune‐related genes significantly differentially expressed in the comparisons of I7/N7 and I14/N14 respectively. Functional annotation revealed that several Gene Ontology (GO) terms related to immunity were significantly enriched between the inoculated and non‐inoculated groups at 14 dpi but not at 7 dpi, despite a similar number of immune‐related genes identified between I7/N7 and I14/N14. The immune response to SE inoculation changes with different time points following SE inoculation. The complicated interaction between the immune system and metabolism contributes to the immune responses to SE inoculation of egg‐type chickens at 14 dpi at the onset of lay. GC, TNFSF8, CD86, CD274, BLB1 and BLB2 play important roles in response to SE inoculation. The results from this study will deepen the current understanding of the genetic response of the egg‐type chicken to SE inoculation at the onset of egg laying.     

番石榴实蝇性别决定基因 Bcotra 和 Bcotra-2 的克隆、序列特征及表达分析

【目的】对番石榴实蝇 Bactrocera correcta (Bezzi)性别决定基因 transformer 和 transformer 2 的cDNA和基因组DNA序列进行克隆和分析,明确这2个基因的结构特征及其在不同发育阶段和雌、雄成虫不同组织中的表达模式,为进一步的功能研究和番石榴实蝇遗传性别品系(genetic sexing strain, GSS)的建立奠定基础。【方法】利用PCR结合RACE技术克隆番石榴实蝇2个性别决定基因的cDNA全长和内含子序列,利用不同的生物信息学软件对序列进行结构预测、序列比对和进化树分析;利用半定量RT-PCR检测这2个基因在番石榴实蝇的不同发育阶段及雌、雄成虫不同组织(精巢、卵巢、中肠和脂肪体)中的表达分布。【结果】克隆得到番石榴实蝇 transformer 和 transformer 2 的cDNA全长序列,分别命名为 Bcotra 和 Bcotra-2 。 Bcotra 存在性别特异剪接,雌虫 Bcotra 的cDNA全长1 673 bp,其开放读码框(ORF)为1 242 bp,编码413个氨基酸(GenBank登录号为KP712876);雄虫Bcotra cDNA全长2 025 bp,比雌虫多2个外显子,但由于外显子上有多个终止密码子,因此,不能编码完整的有功能的Tra蛋白(GenBank登录号为KP712877)。 Bcotra-2 不存在性别特异剪接,cDNA全长1 458 bp,其开放读码框(ORF)为756 bp,编码251个氨基酸,具有RNA结合蛋白的典型特征(GenBank登录号为KM658207)。Bcotra-2有8个外显子,7个内含子。氨基酸序列比对和系统进化关系表明,两个基因的系统发育关系一致,Tra-2与目前已报道的双翅目Tra-2具有很高的同源性,而Tra的保守性较Tra-2要低。半定量RT-PCR结果显示, Bcotra 和 Bcotra-2 在番石榴实蝇的不同发育阶段及雌、雄成虫不同组织中都有表达。【结论】本研究明确了Bcotra 和 Bcotra-2 的基因组DNA和cDNA结构特征,Bcotra 和 Bcotra-2 在番石榴实蝇的不同发育阶段和成虫不同组织中均有表达,序列分析发现这两个性别决定基因均具有Tra/Tra-2结合位点、内含子剪接抑制序列位点,其中 Bcotra 具有RNA结合蛋白的结合位点,暗示了这2个基因可能通过翻译后相互作用调控雌、雄体性发育。Bcotra 存在性别特异剪接,雌虫特有的一段963 bp的内含子序列可以用于番石榴实蝇遗传定性品系的载体构建。     

重楼活性单体pp-10通过抑制PI3K/Akt通路诱导人胃癌细胞BGC-823凋亡和自噬

目的:探讨重楼/七叶一枝花(Paris polyphylla)的醇提物单体pp-10诱导人胃癌BGC-823细胞凋亡和自噬及其分子机制。方法:采用MTT法和克隆形成抑制实验观察不同浓度的重楼单体pp-10对人胃癌BGC-823细胞的增殖抑制作用;Hoechst33342染色法检测pp-10作用于人胃癌BGC-823细胞后细胞核形态的改变;Annexin V-FITC/PI双染法检测细胞凋亡;Western blotting检测重楼单体pp-10对细胞凋亡和自噬相关蛋白Caspase-3、Caspase-9、(ADP-核糖)聚合酶(PARP)、Bax、Bcl-2、LC3、P62以及PI3K/Akt信号通路相关蛋白(Akt、p-Akt、m TOR、p-m TOR、P70s6k、p-P70s6k)表达的影响。结果:重楼单体pp-10能显著抑制BGC-823细胞的生长,作用呈时间-效应关系及剂量-效应关系;克隆形成抑制实验表明随着pp-10浓度的增加,细胞克隆形成逐渐减少,与对照组相比有显著差异;在荧光显微镜下观察可见其细胞核固缩、边聚、裂解等细胞凋亡形态学变化;流式细胞术检测显示,随着作用药物浓度的增高,其凋亡率逐渐升高;Western blotting结果表明,随着药物浓度的增加,线粒体相关凋亡信号通路蛋白Caspase9、Caspase3及PARP均出现酶切活化条带,细胞促凋亡蛋白Bax的表达水平增加,抗凋亡蛋白Bcl-2减少,自噬相关蛋白Ⅱ型LC3增加,P62蛋白减少,p-Akt蛋白的表达水平下降,Akt下游蛋白p-m Tor、p-p70S6K表达减少。结论:重楼单体pp-10通过抑制BGC-823细胞增殖,诱导细胞凋亡和自噬,与下调P13K/Akt信号通路有关。     

microRNA-454-mediated NEDD4-2/TrkA/cAMP axis in heart failure: Mechanisms and cardioprotective implications

The current study aimed to investigate the mechanism by which miR-454 influences the progression of heart failure (HF) in relation to the neural precursor cell expressed, developmentally downregulated 4-2 (NEDD4-2)/tropomyosin receptor kinase A (TrkA)/cyclic adenosine 3',5'-monophosphate (cAMP) axis. Sprague-Dawley rats were used to establish a HF animal model via ligation of the left anterior descending branch of the coronary artery. The cardiomyocyte H9c2 cells were treated with H₂O₂ to stimulate oxidative stress injury in vitro. RT-qPCR and Western blot assay were subsequently performed to determine the expression patterns of miR-454, NEDD4-2, TrkA, apoptosis-related proteins and cAMP pathway markers. Dual-luciferase reporter gene assay coupled with co-immunoprecipitation was performed to elucidate the relationship between miR-454, NEDD4-2 and TrkA. Gain- or loss-of-function experiments as well as rescue experiments were conducted via transient transfection (in vitro) and adenovirus infection (in vivo) to examine their respective functions on H9c2 cell apoptosis and myocardial damage. Our results suggested that miR-454 was aberrantly downregulated in the context of HF, while evidence was obtained suggesting that it targeted NEDD4-2 to downregulate NEDD4-2 in cardiomyocytes. miR-454 exerted anti-apoptotic and protective effects on cardiomyocytes through inhibition of NEDD4-2, while NEDD4-2 stimulated ubiquitination and degradation of TrkA protein. Furthermore, miR-454 activated the cAMP pathway via the NEDD4-2/TrkA axis, which ultimately suppressed cardiomyocyte apoptosis and attenuated myocardial damage. Taken together, the key findings of the current study highlight the cardioprotective role of miR-454, which is achieved through activation of the cAMP pathway by impairing NEDD4-2-induced TrkA ubiquitination.     

Further investigation on nuclear transplantation in different orders of teleost: the combination of the nucleus of Tilapia (Oreochromis nilotica) and the cytoplasm of Loach (Paramisgurnus dabryanus).

The nucleus of a blastula cell from Tilapia (Oreochromis nilotica, family Cichlidae, order Perciformes) was transplanted into an enucleated egg of Loach (Paramisgurnus dabryanus, family Cobitidae, order Cypriniformes). From among 3747 nucleo-cytoplasmic hybrid (NCH) eggs two NCH larval fish (0.05%) were obtained; one died on the 6th day and the other died on the 12th day after the operation. Morphological examinations showed that both NCH larval fish had developed normally with an opened mouth except they could not take food after complete utilization of their egg yolk on the 5th day of development. The possible mechanisms for obtaining such inter-order NCH larval fish are discussed. This is the first report indicating that inter-order NCH larval fish can be obtained in spite of their evolutionary divergence.     

On the causes of trends in the seasonal amplitude of atmospheric CO2

No consensus has yet been reached on the major factors driving the observed increase in the seasonal amplitude of atmospheric CO₂ in the northern latitudes. In this study, we used atmospheric CO₂ records from 26 northern hemisphere stations with a temporal coverage longer than 15 years, and an atmospheric transport model prescribed with net biome productivity (NBP) from an ensemble of nine terrestrial ecosystem models, to attribute change in the seasonal amplitude of atmospheric CO₂. We found significant (p < .05) increases in seasonal peak‐to‐trough CO₂ amplitude (AMP_P‐T) at nine stations, and in trough‐to‐peak amplitude (AMP_T‐P) at eight stations over the last three decades. Most of the stations that recorded increasing amplitudes are in Arctic and boreal regions (>50°N), consistent with previous observations that the amplitude increased faster at Barrow (Arctic) than at Mauna Loa (subtropics). The multi‐model ensemble mean (MMEM) shows that the response of ecosystem carbon cycling to rising CO₂ concentration (eCO₂) and climate change are dominant drivers of the increase in AMP_P‐T and AMP_T‐P in the high latitudes. At the Barrow station, the observed increase of AMP_P‐T and AMP_T‐P over the last 33 years is explained by eCO₂ (39% and 42%) almost equally than by climate change (32% and 35%). The increased carbon losses during the months with a net carbon release in response to eCO₂ are associated with higher ecosystem respiration due to the increase in carbon storage caused by eCO₂ during carbon uptake period. Air‐sea CO₂ fluxes (10% for AMP_P‐T and 11% for AMP_T‐P) and the impacts of land‐use change (marginally significant 3% for AMP_P‐T and 4% for AMP_T‐P) also contributed to the CO₂ measured at Barrow, highlighting the role of these factors in regulating seasonal changes in the global carbon cycle.