果生刺盘孢效应蛋白CfEC92靶向Mal d 1j抑制苹果免疫

由果生刺盘孢引起的炭疽叶枯病是我国苹果产区的重要病害。果生刺盘孢在侵染苹果过程中分泌效应蛋白CfEC92促进其侵染,但其作用机制仍不清楚。本研究从苹果cDNA中克隆出Mal d 1j蛋白,结构域及氨基酸序列分析显示,Mal d 1j为PR10家族成员。Mal d 1j基因过表达能显著增强苹果对炭疽叶枯病抗性,而沉默Mal d 1j显著降低其抗性。在烟草中过表达Mal d 1j提高烟草抗性,共表达CfEC92和Mal d 1j蛋白,降低Mal d 1j对疫霉菌抗性。通过酵母双杂交、BIFC和Co-IP分析证明CfEC92与Mal d 1j可以发生直接互作,且其互作定位于细胞膜和细胞核,表明CfEC92 通过与Mal d 1j互作影响植物免疫。本研究揭示了果生刺盘孢效应蛋白CfEC92通过靶向Mal d 1j抑制植物免疫促进其侵染的分子机制,为苹果炭疽叶枯病防控提供了新的思路。     

中国西藏种子植物区系新资料

本文报道了采自西藏喜马拉雅南坡的8个中国种子植物新记录种以及1个西藏新记录属。前者分别是吉隆牛奶菜(Marsdenia roylei)、塔基棕榈(Trachycarpus takil)、喀西蜂斗草(Sonerila khasiana)、旋花锡生藤(Cissampelos convolvulacea)、吉隆角盘兰(Herminium edgeworthii)、尼泊尔西番莲(Passiflora napalensis)、椭穗姜花(Hedychium ellipticum)和藏南象牙参(Roscoea brandisii); 1个西藏新记录属为箭药藤属(Belostemma) (箭药藤 Belostemma hirsutum)。凭证标本存放于中国科学院西双版纳热带植物园标本馆(HITBC)和西藏自治区高原生物研究所标本室(XZ)。     

微生物相互作用中的空间自组织

微生物在全球生态系统中占据着重要地位, 其中一个重要的研究领域是微生物与环境(包括无机环境与生物环境)之间的相互作用。在生态相互作用过程中, 微生物常常通过自组织形成特定的空间模式。微生物的空间模式在种群稳定性、群落动态变化以及维持合作行为方面具有重要作用。本文中, 我们梳理了当下对微生物空间自组织及其所形成的空间模式的研究内容, 首先介绍什么是空间自组织, 再根据生态相互作用类型对自组织的空间模式进行描述, 其中重点讨论合作与竞争中的空间模式, 接着关注微生物空间自组织的过程, 最后我们指出空间自组织对整个群体的结构和功能稳定具有重要意义。研究微生物种群间相互作用中的空间模式, 有助于探索维持合作行为的新机制, 进而为微生物共生系统的构建提供新的理解。     

睡莲属62个栽培种花朵挥发性成分GC-MS分析北大核心CSCD

为了解睡莲花朵的致香物质,利用气相色谱-质谱法对62个栽培种花朵的挥发性成分进行了研究。结果表明,共检测出72种挥发性成分,以烯烃类(26种)、烷烃类(11种)和醇类(9种)较多,其中花香成分有53种(73.60%)。40个热带睡莲花朵中共检测出56种挥发性成分,其中花香成分39种;22个耐寒睡莲品种花朵共检测出37种挥发性成分,其中花香成分27种。花香成分中主要致香物质有乙酸苄酯、顺式-罗勒烯、苯甲醇、金合欢烯、月桂烯、柠檬烯、苯甲醛、α-异松油稀、α-蒎烯、肉桂醇和β-丁香醇等。利用组内联接余弦的方法,分别根据挥发性成分和花香成分,62个睡莲栽培种(品种)可分成3和4组。这为睡莲香气物质的开发利用及与传粉动物的协同进化研究提供了基础资料。     

Development of a biosensor assessing SARS-CoV-2 main protease proteolytic activity in living cells for antiviral drugs screening

Highlights:
The biosensor reported in our study can monitor SARS-CoV-2 M^pro activity in living cells instead of in vitro solutions.
The biosensor reported in our study is sensitive and easy to operate.
It is suitable for high-throughput screening.
It has the potential to be used in small animal models.     

Two stochastic processes shape diverse senescence patterns in a single‐cell organism

Despite advances in aging research, a multitude of aging models, and empirical evidence for diverse senescence patterns, understanding of the biological processes that shape senescence is lacking. We show that senescence of an isogenic Escherichia coli bacterial population results from two stochastic processes. The first process is a random deterioration process within the cell, such as generated by random accumulation of damage. This primary process leads to an exponential increase in mortality early in life followed by a late age mortality plateau. The second process relates to the stochastic asymmetric transmission at cell fission of an unknown factor that influences mortality. This secondary process explains the difference between the classical mortality plateaus detected for young mothers’ offspring and the near nonsenescence of old mothers’ offspring as well as the lack of a mother–offspring correlation in age at death. We observed that lifespan is predominantly determined by underlying stochastic stage dynamics. Surprisingly, our findings support models developed for metazoans that base their arguments on stage‐specific actions of alleles to understand the evolution of senescence. We call for exploration of similar stochastic influences that shape aging patterns beyond simple organisms.