拟南芥AtR8 lncRNA对盐胁迫响应及其对种子萌发的调节作用

长链非编码RNA (lncRNA)是一类长度大于200个核苷酸且不编码蛋白质的非编码RNA, 主要由RNA聚合酶II转录生成, 大量存在于生物体内并具有多种生物学功能。AtR8 lncRNA是拟南芥(Arabidopsis thaliana)中RNA聚合酶III转录的长链非编码RNA。前期研究发现, 水杨酸(SA)处理诱导萌发种子中AtR8 lncRNA的表达, AtR8 lncRNA缺失抑制SA胁迫下的种子萌发。进一步研究发现, AtR8 lncRNA转录区域内存在保守的盐胁迫响应元件(TCTTCTTCTTTA); NaCl处理抑制萌发种子中AtR8 lncRNA的表达; 与野生型相比, 高浓度NaCl处理明显抑制了atr8 (AtR8 lncRNA部分缺失型拟南芥)种子萌发。研究结果表明, AtR8 lncRNA在拟南芥种子萌发期的盐胁迫中起重要作用。     

水稻根系遗传育种研究进展

根系作为水稻(Oryza sativa)植株的重要组成部分, 在水稻生长发育过程中发挥多种作用, 包括植物的固定、水分和营养物质的获取以及氨基酸和激素的生物合成等, 其形态结构和生理功能与水稻产量和稻米品质以及抗性等密切相关。目前, 通过遗传及生化等诸多手段, 已挖掘到较多水稻根系QTLs与控制基因。该文综述了水稻根系QTL和基因的研究进展, 并对未来根系研究进行展望, 以期为进一步克隆水稻根系基因和完善水稻理想株型模型提供参考。     

Quorum sensing regulation confronts the development of a viable but non-culturable state in Vibrio cholerae

Vibrio cholerae can enter a viable but non-culturable (VBNC) state when it encounters unfavourable environments; VBNC cells serve as important reservoirs and still pose threats to public health. The genetic regulation of V. cholerae entering its VBNC state is not well understood. Here, we show a confrontation strategy adapted by V. cholerae O1 in which it utilizes a quorum sensing (QS) system to prevent transition into a VBNC state under low nutrition and temperature conditions. The upregulation of hapR resulted in a prolonged culturable state of V. cholerae in artificial sea water at 4°C, whereas the mutation of hapR led to fast entry into the VBNC state. We also observed that different V. cholerae O1 natural isolates with distinct QS functions present a variety of abilities to maintain culturability during the transition to a VBNC state. The strain groups with higher or constitutive expression of QS genes exhibit a greater tendency to maintain the culturable state during VBNC induction than those lacking QS functional groups. In summary, HapR-mediated QS regulation is associated with the transition to the VBNC state in V. cholerae. HapR expression causes V. cholerae to resist VBNC induction and become dominant over competitors in changing environments.     

Rice stripe virus coat protein induces the accumulation of jasmonic acid,activating plant defence against the virus while also attracting its vector to feed

The jasmonic acid (JA) pathway plays crucial roles in plant defence against pathogens and herbivores. Rice stripe virus (RSV) is the type member of the genus Tenuivirus. It is transmitted by the small brown planthopper (SBPH) and causes damaging epidemics in East Asia. The role(s) that JA may play in the tripartite interaction against RSV, its host, and vector are poorly understood. Here, we found that the JA pathway was induced by RSV infection and played a defence role against RSV. The coat protein (CP) was the major viral component responsible for inducing the JA pathway. Methyl jasmonate treatment attracted SBPHs to feed on rice plants while a JA-deficient mutant was less attractive than wild-type rice. SBPHs showed an obvious preference for feeding on transgenic rice lines expressing RSV CP. Our results demonstrate that CP is an inducer of the JA pathway that activates plant defence against RSV while also attracting SBPHs to feed and benefitting viral transmission. This is the first report of the function of JA in the tripartite interaction between RSV, its host, and its vector.     

Xanthomonas campestris sensor kinase HpaS co-opts the orphan response regulator VemR to form a branched two-component system that regulates motility

Xanthomonas campestris pv. campestris (Xcc) controls virulence and plant infection mechanisms via the activity of the sensor kinase and response regulator pair HpaS/hypersensitive response and pathogenicity G (HrpG). Detailed analysis of the regulatory role of HpaS has suggested the occurrence of further regulators besides HrpG. Here we used in vitro and in vivo approaches to identify the orphan response regulator VemR as another partner of HpaS and to characterize relevant interactions between components of this signalling system. Bacterial two-hybrid and protein pull-down assays revealed that HpaS physically interacts with VemR. Phos-tag SDS-PAGE analysis showed that mutation in hpaS reduced markedly the phosphorylation of VemR in vivo. Mutation analysis reveals that HpaS and VemR contribute to the regulation of motility and this relationship appears to be epistatic. Additionally, we show that VemR control of Xcc motility is due in part to its ability to interact and bind to the flagellum rotor protein FliM. Taken together, the findings describe the unrecognized regulatory role of sensor kinase HpaS and orphan response regulator VemR in the control of motility in Xcc and contribute to the understanding of the complex regulatory mechanisms used by Xcc during plant infection.