Mitogen-activated protein kinases MPK3 and MPK6 phosphorylate receptor-like cytoplasmic kinase CDL1 to regulate soybean basal immunity.

Soybean cyst nematode (SCN; Heterodera glycines Ichinohe), one of the most devastating soybean (Glycine max) pathogens, causes significant yield loss in soybean production. Nematode infection triggers plant defense responses; however, the components involved in the upstream signaling cascade remain largely unknown. In this study, we established that a mitogen-activated protein kinase (MAPK) signaling module, activated by nematode infection or wounding, is crucial for soybeans to establish SCN resistance. GmMPK3 and GmMPK6 directly interact with CDG1-LIKE1 (GmCDL1), a member of the receptor-like cytoplasmic kinase (RLCK) subfamily VII. These kinases phosphorylate GmCDL1 at Thr-372 to prevent its proteasome-mediated degradation. Functional analysis demonstrated that GmCDL1 positively regulates immune responses and promotes SCN resistance in soybeans. GmMPK3-mediated and GmMPK6-mediated phosphorylation of GmCDL1 enhances GmMPK3 and GmMPK6 activation and soybean disease resistance, representing a positive feedback mechanism. Additionally, 2 L-type lectin receptor kinases, GmLecRK02g and GmLecRK08g, associate with GmCDL1 to initiate downstream immune signaling. Notably, our study also unveils the potential involvement of GmLecRKs and GmCDL1 in countering other soybean pathogens beyond nematodes. Taken together, our findings reveal the pivotal role of the GmLecRKs-GmCDL1-MAPK regulatory module in triggering soybean basal immune responses.

Essential Roles of Cupredoxin Family Proteins in Soybean Cyst Nematode Resistance.

Soybean cyst nematode (SCN, Heterodera glycines), one of the most devastating soybean pathogens, causes a significant yield loss in soybean production. One of the most effective ways to manage SCN is to grow resistant cultivars. Therefore, comparative study using resistant and susceptible soybean cultivars provides a powerful tool to identify new genes involved in soybean SCN resistance. In the present study, a transcriptome analysis was carried out using both the resistant (PI88788) and susceptible (Williams 82) soybean cultivars to characterize the responses to nematode infection. Various defense-related genes and different pathways involved in nematode resistance were recognized as being highly expressed in resistant cultivar. Promoter-GUS analysis was conducted to monitor the spatial expression pattern of the genes highly induced by nematode infection. Two nematode-inducible promoters for Glyma.05g147000 (encoding caffeoyl-CoA O-methyltransferase) and Glyma.06g036700 (encoding cupredoxin superfamily protein) were characterized, and the promoters could efficiently drive the expression of known nematode resistance genes (α-SNAPRhg1HC or GmSHMT) to affect soybean SCN resistance. Interestingly, expression of the cupredoxin family genes was upregulated not only by SCN, but also by jasmonic acid treatment. DNA sequence analysis identified that a conserved motif (GGTGCATG) with high similarity to SCNbox1 and GC-rich element is enriched in their promoter regions, suggesting its potential to serve as a nematode-responsive regulatory element. Overexpression of Glyma.06g036700 significantly enhanced soybean resistance to cyst nematode. Overall, our findings not only highlight the essential role of cupredoxin family genes in SCN resistance, but also offer potential functional tools to develop nematode resistance in crops.