A single nucleotide mutation in GID1c disrupts its interaction with DELLA1 and causes a GA‐insensitive dwarf phenotype in peach

Plant stature is one important factor that affects the productivity of peach orchards. However, little is known about the molecular mechanism(s) underlying the dwarf phenotype of peach tree. Here, we report a dwarfing mechanism in the peach cv. FenHuaShouXingTao (FHSXT). The dwarf phenotype of ‘FHSXT’ was caused by shorter cell length compared to the standard cv. QiuMiHong (QMH). ‘FHSXT’ contained higher endogenous GA levels than did ‘QMH’ and did not response to exogenous GA treatment (internode elongation). These results indicated that ‘FHSXT’ is a GA‐insensitive dwarf mutant. A dwarf phenotype‐related single nucleotide mutation in the gibberellic acid receptor GID1 was identified in ‘FHSXT’ (GID1c^S191F), which was also cosegregated with dwarf phenotype in 30 tested cultivars. GID1c^S191F was unable to interact with the growth‐repressor DELLA1 even in the presence of GA. ‘FHSXT’ accumulated a higher level of DELLA1, the degradation of which is normally induced by its interaction with GID1. The DELLA1 protein level was almost undetectable in ‘QMH’, but not reduced in ‘FHSXT’ after GA₃ treatment. Our results suggested that a nonsynonymous single nucleotide mutation in GID1c disrupts its interaction with DELLA1 resulting in a GA‐insensitive dwarf phenotype in peach.     

lncRNA MALAT1 mediated high glucose–induced HK-2 cell epithelial-to-mesenchymal transition and injury

Journal of Physiology and Biochemistry - Epithelial-to-mesenchymal transition (EMT) and injury of tubular cells play critical roles in the pathogenesis of diabetic nephropathy (DN). lncRNA...     

Design and synthesis of novel 1-phenyl-3-(5-(pyrimidin-4-ylthio)-1,3,4-thiadiazol- 2-yl)urea derivatives with potent anti-CML activity throughout PI3K/AKT signaling pathway

In this investigation, a series of 1-phenyl-3-(5-(pyrimidin-4-ylthio)-1,3,4- thiadiazol-2-yl)urea receptor tyrosine kinase inhibitors were synthesized by a simple and efficient structure-based design. Structure-activity relationship (SAR) analysis of these compounds based on cellular assays led to the discovery of a number of compounds that showed potent activity against human chronic myeloid leukemia (CML) cell line K562, but very weak or no cellular toxicity through monitoring the growth kinetics of K562 cell during a period of 72 h using the real-time live-cell imaging. Among these compounds, 1-(5-((6-((3-morpholinopropyl) amino)pyrimidin-4-yl)thio)-1,3,4-thiadiazol-2-yl)-3-(4-(trifluoromethyl)phenyl)urea (7) exhibited the least cellular toxicity and better biological activity in cellular assays (K562, IC₅₀: 0.038 μM). Compound 7 also displayed very good induced-apoptosis effect for human CML cell line K562 and exerted its effect via a significantly reduced protein phosphorylation of PI3K/Akt signal pathway by Human phospho-kinase array analysis. In vitro results indicate that 1-phenyl-3-(5-(pyrimidin-4-ylthio)-1,3,4- thiadiazol-2-yl)urea derivatives are lead molecules for further development as treatment of chronic myeloid leukemia and cancer.     

Insights into the regulatory characteristics of silkworm fibroin gene promoters using a modified Gal4/UAS system

Transgenic Research - The silkworm Bombyx mori is a valuable insect that synthesizes bulk amounts of fibroin protein in its posterior silk gland (PSG) and weaves these proteins into silk cocoons....     

Hydrogen sulfide alleviates uranium‐induced rat hepatocyte cytotoxicity via inhibiting Nox4/ROS/p38 MAPK pathway

As a gasotransmitter, hydrogen sulfide (H₂S) plays a crucial role in regulating the signaling pathway mediated by oxidative stress. The purpose of this study was to investigate the protective effects of H ₂S on uranium‐induced rat hepatocyte cytotoxicity. Primary hepatocytes were isolated and cultured from Sprague Dawley rat liver tissues. After pretreating with sodium hydrosulfide (an H ₂S donor) for 1 hour (or GKT‐136901 for 30 minutes), hepatocytes were treated by uranyl acetate for 24 hours. Cell viability, reactive oxygen species (ROS), malondialdehyde (MDA), NADPH oxidase 4 (Nox4), and p38 mitogen‐activated protein kinase (p38 MAPK) phosphorylation were respectively determined. The effects of direct inhibition of Nox4 expression by GKT‐136901 (a Nox4 inhibitor) on ROS and phospho‐p38 MAPK levels were examined in uranium‐treated hepatocytes. The results implicate that H ₂S can afford protection of rat hepatocytes against uranium‐induced adverse effects through attenuating oxidative stress via prohibiting Nox4/ROS/p38 MAPK signaling.     

红松和紫椴叶片暗呼吸及其光抑制性在幼、成树间的差异

叶片暗呼吸是森林碳循环的重要组分,深入分析幼、成树的叶片暗呼吸及其光抑制性的差异,对生态系统总生产力(GPP)的准确估算具有重要意义.本研究以长白山阔叶红松林主要树种(红松和紫椴)的幼树和成树为研究对象,分别测算不同光照下叶片暗呼吸与无光暗呼吸,比较叶片暗呼吸及其光抑制性在幼、成树间的差异,结合幼、成树叶片生理生态参数的对比,对幼、成树叶片暗呼吸及其光抑制性差异的原因进行探讨.结果表明: 两个树种幼树叶片光下暗呼吸的值高于成树,在生长季(6—9月),幼树的值比成树高6.8%～39.6%;两个树种幼树叶片暗呼吸光抑制程度低于成树,幼树叶片暗呼吸光抑制性的值比成树低2.5%～14.1%;红松幼、成树间叶片暗呼吸光抑制性的差异总体高于紫椴幼、成树间叶片暗呼吸光抑制性的差异,差值最高可达18.6%;幼树中较高的光下暗呼吸值和较低的光抑制程度可能与最大净光合速率、比叶面积、气孔导度的变化有关,与叶片氮含量的变化无关.     

赖氏衣属,中国地衣一新记录属

报道了文字衣科一中国新记录属——赖氏衣属(Reimnitzia Kalb),该属仅含1种桑蒂赖氏衣[Reimnitzia santensis (Tuck.)Kalb]。桑蒂赖氏衣生于树皮或苔藓上,地衣体壳状,无皮层;含有大的柱状草酸钙结晶;裂芽丰富,与地衣体颜色一致,无分枝,先呈球状,后变为蠕虫状,长度可达1.5 mm,顶部有黑色的孔区或者单个的小孔;具有Chroodiscus型子囊盘;子囊孢子棕色,亚砖壁型,孢子大小15～25μm×8～12μm;分生孢子器位于裂芽的顶端和地衣体疣中,分生孢子呈杆状;无次生代谢物。