Maize rough dwarf disease (MRDD), caused by various species of the genus Fijivirus, threatens maize production worldwide. We previously identified a quantitative locus qMrdd1 conferring recessive resistance to one causal species, rice black-streaked dwarf virus (RBSDV). Here, we show that Rab GDP dissociation inhibitor alpha (RabGDIα) is the host susceptibility factor for RBSDV. The viral P7-1 protein binds tightly to the exon-10 and C-terminal regions of RabGDIα to recruit it for viral infection. Insertion of a helitron transposon into RabGDIα intron 10 creates alternative splicing to replace the wild-type exon 10 with a helitron-derived exon 10. The resultant splicing variant RabGDIα-hel has difficulty being recruited by P7-1, thus leading to quantitative recessive resistance to MRDD. All naturally occurring resistance alleles may have arisen from a recent single helitron insertion event. These resistance alleles are valuable to improve maize resistance to MRDD and potentially to engineer RBSDV resistance in other crops.

Background: The low grain water content (GWC) at harvest is a prerequisite to mechanical harvesting in maize, or otherwise would cause massive broken kernels and increase drying costs. The GWC at harvest in turn depends on GWC at the physiological maturity (PM) stage and grain dehydration rate (GDR). Both GWC and GDR are very complex traits, governed by multiple quantitative trait loci (QTL) and easily influenced by environmental conditions. So far, a number of experiments have been conducted to reveal numbers of GWC and GDR QTL, however, very few QTL have been confirmed, and no QTL has been fine-mapped or even been cloned. Results: We demonstrated that GWCs after PM were positively correlated with GWC at PM, whereas negatively with GDRs after PM. With a recombinant inbred line (RIL) population, we identified totally 31 QTL related to GWC and 17 QTL related to GDR in three field trials. Seven GWC QTL were consistently detected in at least two of the three field trials, each of which could explain 6.92-24.78% of the total GWC variation. Similarly, one GDR QTL was consistently detected, accounting for 9.44-14.46% of the total GDR variation. Three major GWC QTL were found to overlap with three GDR QTL in bins 1.05/06, 2.06/07, and 3.05, respectively. One of the consistent GWC QTL, namely qGwc1.1, was fine-mapped from a 27.22 Mb to a 2.05 Mb region by using recombinant-derived progeny test. The qGwc1.1 acted in a semi-dominant manner to reduce GWC by 1.49-3.31%. Conclusions: A number of consistent GWC and GDR QTL have been identified, and one of them, QTL-qGwc1.1, was successfully refined into a 2.05 Mb region. Hence, it is realistic to clone the genes underlying the GWC and GDR QTL and to make use of them in breeding of maize varieties with low GWC at harvest.

Plants adaptively change their cell wall composition and structure during growth, development, and interactions with environmental stresses. Dirigent proteins (DIRs) contribute to environmental adaptations by dynamically reorganizing the cell wall and/or by generating defense compounds. We established that maize DIR ZmDRR206 (DISEASE RESISTANCE RESPONSE206) mediates maize seedling growth and disease resistance response by coordinately regulating biosynthesis of cell wall components for cell wall integrity (CWI) maintenance. ZmDRR206 responded to pathogen infection by rapidly increasing its expression. Both mutation and overexpression of ZmDRR206 resulted in similar small kernel and diminished seedling growth; while ZmDRR206-overexpression increased disease resistance, greater drought tolerance and reduced photosynthetic activity, thus caused maize seedlings to show a growth-defense trade-off phenotype. Consistently, ZmDRR206-overexpression reduced the contents of primary metabolites and down-regulated the photosynthesis-related genes; while increased the contents of major cell wall components and defense phytohormones; up-regulated defense- and cell wall biosynthesis-related genes in maize seedlings grown under non-stress conditions. Furthermore, ZmDRR206 physically interacted with ZmCesA10, a secondary cell wall-specific cellulose synthase catalytic subunit, in yeast and in planta. Our findings unravel a mechanism that ZmDRR206 maintains CWI during maize seedling growth, providing opportunities for breeding strong disease resistance in maize.

Background Maize rough dwarf disease (MRDD), a widespread disease caused by four pathogenic viruses, severely reduces maize yield and grain quality. Resistance against MRDD is a complex trait that controlled by many quantitative trait loci (QTL) and easily influenced by environmental conditions. So far, many studies have reported numbers of resistant QTL, however, only one QTL have been cloned, so it is especially important to map and clone more genes that confer resistance to MRDD. Results In the study, a major quantitative trait locus (QTL) qMrdd2, which confers resistance to MRDD, was identified and fine mapped. qMrdd2, located on chromosome 2, was consistently identified in a 15-Mb interval between the simple sequence repeat (SSR) markers D184 and D1600 by using a recombinant inbred line (RIL) population derived from a cross between resistant (“80007”) and susceptible (“80044”) inbred lines. Using a recombinant-derived progeny test strategy, qMrdd2 was delineated to an interval of 577 kb flanked by markers N31 and N42. We further demonstrated that qMrdd2 is an incompletely dominant resistance locus for MRDD that reduced the disease severity index by 20.4%. Conclusions A major resistance QTL (qMrdd2) have been identified and successfully refined into 577 kb region. This locus will be valuable for improving maize variety resistance to MRDD via marker-assisted selection (MAS).

Plants adaptively change their cell wall composition and structure during their growth, development, and interactions with environmental stresses. Dirigent proteins (DIRs) contribute to environmental adaptations by dynamically reorganizing the cell wall and/or by generating defense compounds. Here, we established that maize DIR, ZmDRR206, mediates maize seedling growth and disease resistance by coordinately regulating biosynthesis of cell wall components for cell wall integrity (CWI) maintenance. The expression of ZmDRR206 increased rapidly in maize seedling upon pathogen infection. Both overexpression and mutation of ZmDRR206 resulted in small kernel and diminished seedling growth; while ZmDRR206-overexpression increased disease resistance, enhanced drought tolerance and reduced photosynthetic activity, thus caused the maize seedlings to show a growth and defense trade-off phenotype. Consistently, ZmDRR206-overexpression reduced the contents of primary metabolites and down-regulated the photosynthesis-related genes; while increased the contents of major cell wall components and defense phytohormones and up-regulated defense- and cell wall biosynthesis-related genes in maize seedlings grown under non-stress conditions. Furthermore, ZmDRR206 physically interacted with ZmCesA10 in yeast and in planta. Our findings unravel a mechanism that ZmDRR206 coordinately regulates biosynthesis of cell wall components for CWI maintenance during maize seedling growth, providing opportunities for breeding strong disease resistance in maize.