Abstract

Legume biological nitrogen fixation (BNF) is the most important N source in agricultural ecosystems. Nodule organogenesis from the primordia to the development of mature nodules with the ability to fix N2 largely determines BNF capacity. However, nodule growth is often limited by low phosphorus (P) availability, while the mechanisms underlying nodule development responses to P deficiency remain largely unknown. In this study, we found that nodule enlargement is severely inhibited by P deficiency, as reflected by the smaller individual nodule size from a soybean core collection in the field. Wide-ranging natural diversity in nodule size was further identified in soybeans reared in low P soils, with the FC-1 genotype outperforming FC-2 in assessments of nodulation under low P conditions. Among β-expansin members, GmINS1 expression is most abundantly enhanced by P deficiency in FC-1 nodules, and its transcript level is further displayed to be tightly associated with nodule enlargement. Four single nucleotide polymorphisms discovered in the GmINS1 promoter distinguished the FC-1 and FC-2 genotypes and accounted for the differential expression levels of GmINS1 responses to P deficiency. GmINS1 overexpression led to increases in nodule size, infected cell abundance, and N2 fixation capacity and subsequently promoted increases in N and P content, soybean biomass and yield. Our findings provide a candidate gene for optimizing BNF capacity responses to low P stress in soybean molecular breeding programs. This article is protected by copyright. All rights reserved.

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