Fluorescent Soybean Hairy Root Construction and Its Application in the Soybean—Nematode Interaction: An Investigation

SIMPLE SUMMARY: The soybean cyst nematode is a pathogen that is parasitic on soybean roots and causes high yield losses. To control it, it is necessary to study resistance genes and their mechanisms. The existing means take half a year but our new method can accelerate the process. We built new tools and integrated the advantages of current technologies to develop an FHR-SCN system. This method shortens the experimental period from half a year to six weeks. Researchers can differentiate between the roots that are transgenic and those that are not with a blue light flashlight and filter. Using this method, we verified a gene that could provide an additional contribution to resistance against the nematode. In addition, we used a transgenic soybean to verify and further indicate that this resistance was caused by an increase of jasmonic acid. The FHR-SCN pathosystem will accelerate the study of the soybean resistant gene. ABSTRACT: Background: The yield of soybean is limited by the soybean cyst nematode (SCN, Heterodera glycines). Soybean transformation plays a key role in gene function research but the stable genetic transformation of soybean usually takes half a year. Methods: Here, we constructed a vector, pNI-GmUbi, in an Agrobacterium rhizogenes-mediated soybean hypocotyl transformation to induce fluorescent hairy roots (FHRs). Results: We describe the operation of FHR-SCN, a fast, efficient and visual operation pathosystem to study the gene functions in the soybean-SCN interaction. With this method, FHRs were detected after 25 days in 4 cultivars (Williams 82, Zhonghuang 13, Huipizhiheidou and Peking) and at least 66.67% of the composite plants could be used to inoculate SCNs. The demographics of the SCN could be started 12 days post-SCN inoculation. Further, GmHS1(pro-1) was overexpressed in the FHRs and GmHS1(pro-1) provided an additional resistance in Williams 82. In addition, we found that jasmonic acid and JA-Ile increased in the transgenic soybean, implying that the resistance was mainly caused by affecting the content of JA and JA-Ile. Conclusions: In this study, we established a pathosystem, FHR-SCN, to verify the functional genes in soybeans and the SCN interaction. We also verified that GmHS1(pro-1) provides additional resistance in both FHRs and transgenic soybeans, and the resistance may be caused by an increase in JA and JA-Ile contents.