qMrdd2, a novel quantitative resistance locus for maize rough dwarf disease.

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).

Genetic dissection of grain water content and dehydration rate related to mechanical harvest in maize.

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.

ZmGDIα-hel counters the RBSDV-induced reduction of active gibberellins to alleviate maize rough dwarf virus disease.

Maize rough dwarf disease (MRDD) threatens maize production globally. The P7-1 effector of the rice black-streaked dwarf virus (RBSDV) targets maize Rab GDP dissociation inhibitor alpha (ZmGDIα) to cause MRDD. However, P7-1 has difficulty recruiting a ZmGDIα variant with an alternative helitron-derived exon 10 (ZmGDIα-hel), resulting in recessive resistance. Here, we demonstrate that P7-1 can recruit another maize protein, gibberellin 2-oxidase 13 (ZmGA2ox7.3), which also exhibits tighter binding affinity for ZmGDIα than ZmGDIα-hel. The oligomerization of ZmGA2ox7.3 is vital for its function in converting bioactive gibberellins into inactive forms. Moreover, the enzymatic activity of ZmGA2ox7.3 oligomers increases when forming hetero-oligomers with P7-1/ZmGDIα, but decreases when ZmGDIα-hel replaces ZmGDIα. Viral infection significantly promotes ZmGA2ox7.3 expression and oligomerization in ZmGDIα-containing susceptible maize, resulting in reduced bioactive GA1/GA4 levels. This causes an auxin/cytokinin imbalance and ultimately manifests as MRDD syndrome. Conversely, in resistant maize, ZmGDIα-hel counters these virus-induced changes, thereby mitigating MRDD severity.

The ZmWAKL-ZmWIK-ZmBLK1-ZmRBOH4 module provides quantitative resistance to gray leaf spot in maize.

Gray leaf spot (GLS), caused by the fungal pathogens Cercospora zeae-maydis and Cercospora zeina, is a major foliar disease of maize worldwide (Zea mays L.). Here we demonstrate that ZmWAKL encoding cell-wall-associated receptor kinase-like protein is the causative gene at the major quantitative disease resistance locus against GLS. The ZmWAKLY protein, encoded by the resistance allele, can self-associate and interact with a leucine-rich repeat immune-related kinase ZmWIK on the plasma membrane. The ZmWAKLY/ZmWIK receptor complex interacts with and phosphorylates the receptor-like cytoplasmic kinase (RLCK) ZmBLK1, which in turn phosphorylates its downstream NADPH oxidase ZmRBOH4. Upon pathogen infection, ZmWAKLY phosphorylation activity is transiently increased, initiating immune signaling from ZmWAKLY, ZmWIK, ZmBLK1 to ZmRBOH4, ultimately triggering a reactive oxygen species burst. Our study thus uncovers the role of the maize ZmWAKL-ZmWIK-ZmBLK1-ZmRBOH4 receptor/signaling/executor module in perceiving the pathogen invasion, transducing immune signals, activating defense responses and conferring increased resistance to GLS.

A helitron-induced RabGDIα variant causes quantitative recessive resistance to maize rough dwarf disease.

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.