At3g53630 encodes a GUN1-interacting protein under norflurazon treatment

Chloroplasts are semi-autonomous organelles, with more than 95% of their proteins encoded by the nuclear genome. The chloroplast-to-nucleus retrograde signals are critical for the nucleus to coordinate its gene expression for optimizing or repairing chloroplast functions in response to changing environments. In chloroplasts, the pentatricopeptide-repeat protein GENOMES UNCOUPLED 1 (GUN1) is a master switch that senses aberrant physiological states, such as the photooxidative stress induced by norflurazon (NF) treatment, and represses the expression of photosynthesis-associated nuclear genes (PhANGs). However, it is largely unknown how the retrograde signal is transmitted beyond GUN1. In this study, a protein GUN1-INTERACTING PROTEIN 1 (GIP1), encoded by At3g53630, was identified to interact with GUN1 by different approaches. We demonstrated that GIP1 has both cytosol and chloroplast localizations, and its abundance in chloroplasts is enhanced by NF treatment with the presence of GUN1. Our results suggest that GIP1 and GUN1 may function antagonistically in the retrograde signaling pathway.

     

肺部微生物组通过炎症反应介导慢性阻塞性肺疾病转化为肺癌的研究进展

肺部微生物组存在于呼吸道和实质组织中,通过菌群紊乱、代谢产物、炎症反应、免疫反应、基因毒性等方面介导肺部损伤。随着肺部微生物组的深入研究,发现肺部微生物组的相关活动与慢性阻塞性肺疾病(chronic obstructive pulmonary disease, COPD)和肺癌息息相关,能够促使COPD向肺癌的转变。本文主要介绍了肺部微生物组稳态及其通过炎症反应导致COPD和肺癌,重点探讨了肺部微生物组如何通过炎症反应介导COPD转化为肺癌,以期为COPD和肺癌的临床预防、优化治疗以及新型药物设计提供新的理论依据。     

MicroRNA-197-3p mediates damage to human coronary artery endothelial cells via targeting TIMP3 in Kawasaki disease

Kawasaki disease (KD) causes cardiovascular system injury in children. However, the pathogenic mechanisms of KD have not been well defined. Recently, strong correlation between aberrant microRNAs and KD nosogenesis has been revealed. A role of microRNA-197-3p (miR-197-3p) in the pathogenesis of KD is identified in the present study. Cell proliferation assay showed human coronary artery endothelial cells (HCAECs) were suppressed by serum from KD patients, which was correlated with high levels of miR-197-3p in both KD serum and HCAECs cultured with KD serum. The inhibition of HCAECs by miR-197-3p was confirmed by cells expressing miR-197-3p mimic and miR-197-3p inhibitor. Comparative proteomics analysis and Ingenuity Pathway Analysis (IPA) revealed TIMP3 as a potential target of miR-197-3p, which was demonstrated by western blot and dual-luciferase reporter assays. Subsequently, by detecting the endothelium damage markers THBS1, VWF, and HSPG2, the role of miR-197-3p/TIMP3 in KD-induced damage to HCAECs was confirmed, which was further validated by a KD mouse model in vivo. The expressions of miR-197-3p and its target, TIMP3, are dramatically variational in KD serum and HCAECs cultured with KD serum. Increased miR-197-3p induces HCAECs abnormal by restraining TIMP3 expression directly. Hence, dysregulation of miR-197-3p/TIMP3 expression in HCAECs may be an important mechanism in cardiovascular endothelium injury in KD patients, which offers a feasible therapeutic target for KD treatment.

     

Cell-type action specificity of auxin on Arabidopsis root growth

The plant hormone auxin plays a critical role in root growth and development; however, the contributions or specific roles of cell-type auxin signals in root growth and development are not well understood. Here, we mapped tissue and cell types that are important for auxin-mediated root growth and development by manipulating the local response and synthesis of auxin. Repressing auxin signaling in the epidermis, cortex, endodermis, pericycle or stele strongly inhibited root growth, with the largest effect observed in the endodermis. Enhancing auxin signaling in the epidermis, cortex, endodermis, pericycle or stele also caused reduced root growth, albeit to a lesser extent. Moreover, we established that root growth was inhibited by enhancement of auxin synthesis in specific cell types of the epidermis, cortex and endodermis, whereas increased auxin synthesis in the pericycle and stele had only minor effects on root growth. Our study thus establishes an association between cellular identity and cell type-specific auxin signaling that guides root growth and development.     

耐高盐枯草芽孢杆菌XP合成球形纳米硒及其抑制草莓病原真菌生物活性

生物方法合成纳米材料具有低能耗、高安全性以及环境友好等优良特点,因而备受人们关注。利用细菌将硒酸盐或亚硒酸盐还原为单质硒,不仅可以降低硒毒性,而且还能获得价值更高的生物纳米材料。文中选用可耐受高盐环境胁迫的枯草芽孢杆菌亚种Bacillus subtilis subspecies stercoris strain XP构建生物模型,分别以LB液体培养基和亚硒酸钠为介质和底物 (电子受体),解析菌株XP合成纳米硒的基本规律。通过扫描电镜 (Scanning electron microscope,SEM) 观察、X射线能谱分析 (X-ray energy dispersive spectral analysis,EDAX)、X射线衍射 (X-ray diffraction,XRD) 分析、傅里叶红外变换光谱 (Fourier transform infrared spectroscopy,FTIR) 技术对合成的纳米硒进行物理化学表征分析,同时选用草莓枯萎、红叶、紫斑病病原真菌对其抗菌活性进行分析。结果表明,菌株XP介导合成的单质硒为球形纳米颗粒 (Selenium nanoparticles,SeNPs),其生成量与反应时间呈正相关 (0–48 h),且细胞形态未发生褶皱或破损等变化 (耐受力强);SeNPs为非晶态,粒径范围在135–165 nm,表面元素组成以Se为主,同时存在C、O、N、S等有机元素;颗粒表面包裹生物大分子物质,-OH、C=O、N-H、C-H等官能团与SeNPs稳定性和生物活性密切相关;高浓度纳米硒对枯萎、红叶、紫斑病病原真菌均有显著抑制活性 (P<0.05),其中对草莓红叶病与枯萎病病原真菌的抑制活性明显优于对紫斑病病原真菌的抑制活性。总而言之,菌株XP不仅耐受高盐胁迫能力强,同时还可介导合成生物SeNPs,其合成的纳米硒颗粒具有良好的稳定性和生物活性,在草莓病害防治以及绿色富硒草莓种植等领域具有潜在的应用价值。     

Kunitz型丝氨酸蛋白酶抑制剂研究进展

Kunitz型丝氨酸蛋白酶抑制剂是一类普遍存在的蛋白酶抑制剂,在体内各项生命活动中扮演着重要角色。这类抑制剂结构稳定且富有特色,通常具有一个或几个串联存在的Kunitz结构域,能够以类似底物的方式与丝氨酸蛋白酶结合,从而抑制酶的活性。在功能方面,Kunitz型丝氨酸蛋白酶抑制剂参与凝血和纤维蛋白溶解、肿瘤免疫、炎症调节以及抵抗细菌、真菌感染等过程。文中就Kunitz型丝氨酸蛋白酶抑制剂研究进展作一综述,为新型Kunitz型丝氨酸蛋白酶抑制剂的开发提供研究思路。