栽培菊花与菊属-近缘属属间杂种杂交后代耐盐性的遗传分析

为了解菊花近缘种属植物耐盐性的遗传规律,对栽培菊花与菊属-近缘属属间杂种杂交后代耐盐性进行了遗传分析。以栽培菊花'韩2’为母本,大岛野路菊×芙蓉菊属间杂种为父本进行杂交,以盐害指数作为指标,通过水培法对获得的F₁群体进行耐盐性鉴定,并应用植物数量性状主基因+多基因混合遗传模型,采用单个F₂世代的分离分析方法对F₁群体耐盐性进行混合遗传分析。结果发现:F₁群体的耐盐性出现广泛分离,变异系数达53.63%,盐害指数的变异范围为3.33%-96.67%;中亲优势为2.47,未达到显著水平;将后代的耐盐性分为5个级别,其中高耐的占14.52%,耐盐的占38.70%,中耐的占30.65%,敏盐的占9.68%,高敏的占6.45%。F₁群体的耐盐性符合B-2模型,由两个主效基因控制,加性效应均表现正向增效,分别为18.06和19.13,显性效应表现负向效应,分别为-17.99和-1.44,主基因遗传率为61.14%,属高度遗传力。综合分析表明:菊花近缘种属植物耐盐性可通过杂交导入栽培菊花,实现栽培菊花耐盐性遗传改良;菊花近缘种属植物盐害指数受两对主基因的控制,主基因在F₁群体的遗传率属高度遗传力,耐盐性选育可在早期世代进行。     

瘦蛋白介导的AMPK信号转导途径

瘦蛋白(leptin)介导的腺苷酸激活蛋白激酶(AMP-activated protein kinase,AMPK)信号转导途径在脂肪代谢的调节中起重要作用。瘦蛋白与其受体结合使AMPK信号转导途径激活,最终激活肉碱脂酰转移酶-1,通过促进脂肪酸氧化而参与脂肪代谢的调节。本文主要介绍近年来关于瘦蛋白介导的AMPK信号转导途径的组成、活性调节及其作用机制的最新研究进展。     

Construction of Ordered Atomic Donor–Acceptor Architectures in bcc IrGa Intermetallic Compounds toward Highly Electroactive and Stable Overall Water Splitting

Benefiting from ordered atomic structures and strong d-orbital interactions, intermetallic compounds (IMCs) are promising electrocatalysts for hydrogen evolution reaction (HER) and oxygen evolution reaction (OER). Herein, the body-centered cubic IrGa IMCs with atomic donor–acceptor architectures are synthesized and anchored on the nitrogen-doped reduced graphene oxide (i.e., IrGa/N-rGO). Structural characterizations and theoretical calculations reveal that the electron-rich Ir sites are atomically dispersed in IrGa/N-rGO, facilitating the electron transfer between Ir atoms and adsorbed species, which can efficiently decrease the energy barriers of the potential determining step for both HER and OER. Impressively, the IrGa/N-rGO||IrGa/N-rGO exhibits excellent performance for overall water splitting in alkaline medium, requiring a low cell voltage of 1.51 V to achieve 10 mA cm⁻², meanwhile, exhibiting no significant degradation for 100 h. This work demonstrates that the rational design of noble metal electrocatalysts with donor–acceptor architectures is beneficial for catalytic reactions in energy conversion applications.     

长江口外低氧区及其邻近海域表层沉积物反硝化微生物多样性和分布特征

[目的]微生物参与的反硝化是河口区氮损失的主要途径.[方法]本研究采用Illumina MiSeq测序方法,研究了长江口外低氧区及其邻近海域表层沉积物中nirS型和nirK型反硝化微生物群落的多样性和分布特征.[结果]样品共检测到346个nirS Operational Taxonomic Units和267个nirK...     

Inhibition of the sonic hedgehog pathway activates TGF-β-activated kinase (TAK1) to induce autophagy and suppress apoptosis in thyroid tumor cells

The sonic hedgehog (Shh) pathway is highly activated in a variety of malignancies and plays important roles in tumorigenesis, tumor growth, drug resistance, and metastasis. Our recent study showed that the inhibitors of the Shh pathway such as cyclopamine (CP), a Smothened (SMO) inhibitor, and GANT61, a Gli1 inhibitor, have modest inhibitory effects on thyroid tumor cell proliferation and tumor growth. The objective of this study was to determine whether autophagy was induced by inhibition of the Shh pathway and could negatively regulate GANT61-induced apoptosis. Here we report that inhibition of the Shh pathway by Gli1 siRNA or by cyclopamine and GANT61 induced autophagy in SW1736 and KAT-18 cells, two anaplastic thyroid cancer cell lines; whereas Gli1 overexpression suppressed autophagy. Mechanistic investigation revealed that inhibition of the Shh pathway activated TAK1 and its two downstream kinases, the c-Jun-terminal kinase (JNK) and AMP-activated protein kinase (AMPK). GANT61-induced autophagy was blocked by TAK1 siRNA and the inhibitors of TAK1 (5Z-7-oxozeaenol, 5Z), JNK (SP600125), and AMPK (Compound C, CC). Inhibition of autophagy by chloroquine and 5Z and by TAK1 and Beclin-1 siRNA enhanced GANT61-induced apoptosis and its antiproliferative activity. Our study has shown that inhibition of the Shh pathway induces autophagy by activating TAK1, whereas autophagy in turn suppresses GANT61-induced apoptosis. We have uncovered a previously unrecognized role of TAK1 in Shh pathway inhibition-induced autophagy and apoptosis.Subject terms: Thyroid cancer, Macroautophagy, Apoptosis, Drug development