Sclerotinia stem rot, caused by Sclerotinia sclerotiorum, is a destructive soil-borne disease leading to huge yield loss. We previously reported that Klebsiella variicola FH-1 could degrade atrazine herbicides, and the vegetative growth of atrazine-sensitive crops (i.e., soybean) was significantly increased in the FH-1-treated soil. Interestingly, we found that FH-1 could promote soybean growth and induce resistance to S. sclerotiorum. In our study, strain FH-1 could grow in a nitrogen-free environment, dissolve inorganic phosphorus and potassium, and produce indoleacetic acid and a siderophore. The results of pot experiments showed that K. variicola FH-1 promoted soybean plant development, substantially improving plant height, fresh weight, and root length, and induced resistance against S. sclerotiorum infection in soybean leaves. The area under the disease progression curve (AUDPC) for treatment with strain FH-1 was significantly lower than the control and was reduced by up to 42.2% within 48 h (P<0.001). Moreover, strain FH-1 rcovered the activities of catalase, superoxide dismutase, peroxidase, phenylalanine ammonia lyase, and polyphenol oxidase, which are involved in plant protection, and reduced malondialdehyde accumulation in the leaves. The mechanism of induction of resistance appeared to be primarily resulted from the enhancement of transcript levels of PR10, PR12, AOS, CHS, and PDF1.2 genes. The colonization of FH-1 on soybean root, determined using CLSM and SEM, revealed that FH-1 colonized soybean root surfaces, root hairs, and exodermis to form biofilms. In summary, K. variicola FH-1 exhibited the biological control potential by inducing resistance in soybean against S. sclerotiorum infection, providing new suggestions for green prevention and control.
N6-methyladenosine (m6A) plays a key role in mammalian early embryonic development and cell lineage differentiation. However, the role and mechanisms of 18S ribosomal RNA (rRNA) m6A methyltransferase METTL5 in early embryonic development remain unclear. Here, we found that 18S rRNA m6A methyltransferase METTL5 plays an important role in porcine early embryonic development. METTL5 knockdown and overexpression significantly reduced the developmental efficiency of porcine early embryos and impaired cell lineage allocation. METTL5 knockdown apparently decreased the global translation efficiency in blastocyst, while METTL5 overexpression increased the global translation efficiency. Furthermore, METTL5 knockdown did not affect the abundance of CDX2 mRNA, but resulted in a significant reduction in CDX2 protein levels. Moreover, the low developmental efficiency and abnormal lineage distribution of METTL5 knockdown embryos could be rescued by CDX2 overexpression. Collectively, our results demonstrated that 18S rRNA methyltransferase METTL5 regulates porcine early embryonic development via modulating the translation of CDX2.