Plants use their innate immune system to defend against phytopathogens. As a part of this, pattern triggered-immunity is activated via pattern recognition receptor (PRR) detection of pathogen-associated molecular patterns (PAMPs). Although an increasing number of PAMPs have been identified, the PRRs for their recognition remain largely unknown. In the present study, we report a receptor-like protein RE02 (Response to VmE02) in Nicotiana benthamiana, which mediates the perception of VmE02, a PAMP previously identified from the phytopathogenic fungus Valsa mali, using virus-induced gene silencing (VIGS), co-immunoprecipitation, pull-down and microscale thermophoresis assays. We show that silencing of RE02 markedly attenuated VmE02-triggred cell death and immune responses. RE02 specifically interacted with VmE02 in vivo and in vitro, and it displayed a high affinity for VmE02. Formation of a complex with the receptor-like kinases SOBIR1 and BAK1 was essential for RE02 to perceive VmE02. Moreover, RE02-silenced plants exhibited enhanced susceptibility to both the oomycete Phytophthora capsici and the fungus Sclerotinia sclerotiorum, while overexpression of RE02 increased plant resistance to these pathogens. Together, our results indicate that the PAMP VmE02 and the receptor-like protein RE02 represent a new ligand-receptor pair in plant immunity, and that RE02 represents a promising target for engineering disease resistance.

In recent years, the important role of long noncoding RNAs (lncRNAs) in the development of liver cancer has received increasing attention. The abnormal expression level of long non-coding RNAs has been associated with the occurrence and development of liver cancer. However, the role and molecular mechanisms of lncRNAs in the development and progression of liver cancer are not fully understood. The present study aimed to clarify the function and molecular mechanism of lncRNA brain cytoplasmic 200 (BC200) in liver cancer. In the present study, it was found that BC200 expression level was higher in hepatocellular carcinoma (HCC) tissues than that in adjacent tissues. Cell function was examined by constructing BC200 knockout (KO) and BC200-overexpression in vitro models. It was found that BC200 affected the proliferation and migration of HepG2 cells. Interestingly, it was found that BC200 affected the expression of c-Myc protein but did not affect the mRNA expression level of c-MYC. BC200 KO cells exhibited a reduced protein expression level of Bax protein and an increased protein expression level of Bcl-xL. Conversely, BC200 overexpression reduced the expression of Bcl-xL protein and increased the expression of Bax protein. Importantly, it was found that BC200 affected the formation of subcutaneous tumors in nude mice. In conclusion, the present results suggested that lncRNA BC200 may play an important role in liver cancer.