热带滨海植物红厚壳的抗逆生物学特性

为了解红厚壳(Calophyllum inophyllum)的抗逆特性,对西沙群岛自然生长的红厚壳叶片的形态解剖、生理生态、以及叶片和适生土壤的元素含量进行了研究。结果表明,红厚壳是阳生性植物,其上表皮厚,海绵组织发达且栅栏组织排列紧密,气孔排列松散且密度小(24.40 mm~(-2)),有利于叶片保水抵御干旱。叶片的叶绿素a、b含量低(分别为0.87和0.43 mg g~(-1)),表明红厚壳具适应强光环境的能力。叶片的MDA含量低(13.46 nmol g~(-1)),PRO含量高(127.89μg g~(-1)),SOD活性高(149.42 U g~(-1)),总抗氧化能力高(388.60 U g~(-1)),显示红厚壳能通过提高自身的抗氧化能力抵御膜脂过氧化伤害。红厚壳自然生长的珊瑚岛土壤较为贫瘠、营养元素含量低,但红厚壳植株体内具有较高的营养元素含量,表明红厚壳营养元素利用率高,对于贫瘠土壤具有很好的适应能力。因此,红厚壳具有较高的抗氧化胁迫能力和耐受干旱的能力,适宜生长在热带珊瑚岛等土壤贫瘠的生境,可以作为热带珊瑚岛防风固沙和植被恢复的工具种。     

基因前定点敲入FLAG标签表达的FLAG-SND1蛋白参与胞内应激颗粒的形成

CRISPR/Cas9 (clustered regularly interspaced short palindromic repeats-Cas9 nuclease) 基因编辑技术是近年来新兴的一种可以实现基因特异性敲除和敲入的技术。本文利用CRISPR/Cas9基因编辑系统,将3×FLAG标签定点敲入HeLa细胞SND1基因前方,使细胞内源性表达的SND1蛋白带有3×FLAG标签,并观察SND1与应激颗粒及加工体的定位情况。设计针对SND1基因起始密码子ATG附近的sgRNA,以px459为表达载体,构建出重组真核表达质粒。设计含有3×FLAG及待插入位置上下游150 bp同源臂的序列,经公司合成获得重组质粒。将2个质粒共同转染HeLa细胞,使用嘌呤霉素筛选阳性细胞,挑取单克隆后培养。Western 印迹表明,细胞表达3×FLAG-SND1融合蛋白质。提取细胞基因组DNA进行测序。测序无误获得稳定株后,用流式细胞术检测细胞周期和凋亡,发现与WT细胞相比无显著性差异。同时,使用0.5 mmol/L亚砷酸钠处理,细胞发生氧化应激,eIF2α蛋白磷酸化增加,胞浆中出现应激颗粒,SND1与应激颗粒标志蛋白TIAR存在共定位现象,但不存在与加工体蛋白DCP1α的共定位。     

Parabacteroides distasonis Alleviates Obesity and Metabolic Dysfunctions via Production of Succinate and Secondary Bile Acids

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植物TOR激酶响应上游信号的研究进展

雷帕霉素靶蛋白(TOR)是真核生物中高度保守的丝氨酸/苏氨酸蛋白激酶, 能整合营养、能量、生长因子及环境信号, 协调细胞增殖、生长和代谢等过程, 是真核生物生长发育的核心调控因子。近年来, 随着相关研究系统的建立, 植物TOR的功能和机制研究取得了众多突破, 发现其进化上保守的生物学功能及植物中特有的信号通路。该文概述了TOR蛋白复合体的构成, 以及植物TOR响应糖、营养元素(氮、磷和硫)、激素及逆境胁迫信号来调控下游基因转录、蛋白翻译、代谢、细胞自噬和胁迫应答等生物学过程的分子机制, 并提出了植物TOR领域一些亟待解决的科学问题, 以期为全面揭示植物TOR的生物学功能提供参考。     

Genomic insights into the adaptation and evolution of the nautilus,an ancient but evolving “living fossil”

The nautilus, commonly known as a “living fossil,” is endangered and may be at risk of extinction. The lack of genomic information hinders a thorough understanding of its biology and evolution, which can shed light on the conservation of this endangered species. Here, we report the first high-quality chromosome-level genome assembly of Nautilus pompilius. The assembled genome size comprised 785.15 Mb. Comparative genomic analyses indicated that transposable elements (TEs) and large-scale genome reorganizations may have driven lineage-specific evolution in the cephalopods. Remarkably, evolving conserved genes and recent TE insertion activities were identified in N. pompilius, and we speculate that these findings reflect the strong adaptability and long-term survival of the nautilus. We also identified gene families that are potentially responsible for specific adaptation and evolution events. Our study provides unprecedented insights into the specialized biology and evolution of N. pompilius, and the results serve as an important resource for future conservation genomics of the nautilus and closely related species.     

hPEBP4 resists TRAIL-induced apoptosis of human prostate cancer cells by activating Akt and deactivating ERK1/2 pathways

The treatment options available for prostate cancer are limited because of its resistance to therapeutic agents. Thus, a better understanding of the underlying mechanisms of the resistance of prostate cancer will facilitate the discovery of more efficient treatment protocols. Human phosphatidylethanolamine-binding protein 4 (hPEBP4) is recently identified by us as an anti-apoptotic molecule and a potential candidate target for breast cancer treatment. Here we found the expression levels of hPEBP4 were positively correlated with the severity of clinical prostate cancer. Furthermore, hPEBP4 was not expressed in TRAIL-sensitive DU145 prostate cancer cells, but was highly expressed in TRAIL-resistant LNCaP cells, which show highly activated Akt. Interestingly, hPEBP4 overexpression in TRAIL-sensitive DU145 cells promoted Akt activation but inhibited ERK1/2 activation. The hPEBP4-overexpressing DU145 cells became resistant to TRAIL-induced apoptosis consequently, which could be reversed by PI3K inhibitors. In contrast, silencing of hPEBP4 in TRAIL-resistant LNCaP cells inhibited Akt activation but increased ERK1/2 activation, resulting in their sensitivity to TRAIL-induced apoptosis that was restored by the MEK1 inhibitor. Therefore, hPEBP4 expression in prostate cancer can activate Akt and deactivate ERK1/2 signaling, leading to TRAIL resistance. We also demonstrated that hPEBP4-mediated resistance to TRAIL-induced apoptosis occurred downstream of caspase-8 and at the level of BID cleavage via the regulation of Akt and ERK pathways, and that hPEBP4-regulated ERK deactivation was upstream of Akt activation in prostate cancer cells. Considering that hPEBP4 confers cellular resistance to TRAIL-induced apoptosis and is abundantly expressed in poorly differentiated prostate cancer, silencing of hPEBP4 suggests a promising approach for prostate cancer treatment.