The postdomestication adaptation of maize to longer days required reduced photoperiod sensitivity to optimize flowering time. We performed a genome-wide association study and confirmed that ZmCCT, encoding a CCT domain-containing protein, is associated with the photoperiod response. In early-flowering maize we detected a CACTA-like transposable element (TE) within the ZmCCT promoter that dramatically reduced flowering time. TE insertion likely occurred after domestication and was selected as maize adapted to temperate zones. This process resulted in a strong selective sweep within the TE-related block of linkage disequilibrium. Functional validations indicated that the TE represses ZmCCT expression to reduce photoperiod sensitivity, thus accelerating maize spread to long-day environments.

Head smut is a systemic disease in maize caused by the soil-borne fungus Sporisorium reilianum that poses a grave threat to maize production worldwide. A major head smut quantitative resistance locus, qHSR1, has been detected on maize chromosome bin2.09. Here we report the map-based cloning of qHSR1 and the molecular mechanism of qHSR1-mediated resistance. Sequential fine mapping and transgenic complementation demonstrated that ZmWAK is the gene within qHSR1 conferring quantitative resistance to maize head smut. ZmWAK spans the plasma membrane, potentially serving as a receptor-like kinase to perceive and transduce extracellular signals. ZmWAK was highly expressed in the mesocotyl of seedlings where it arrested biotrophic growth of the endophytic S. reilianum. Impaired expression in the mesocotyl compromised ZmWAK-mediated resistance. Deletion of the ZmWAK locus appears to have occurred after domestication and spread among maize germplasm, and the ZmWAK kinase domain underwent functional constraints during maize evolution.

Cytoplasmic actin cables are the most prominent actin structures in plant cells, but the molecular mechanism underlying their formation is unknown. The function of these actin cables, which are proposed to modulate cytoplasmic streaming and intracellular movement of many organelles in plants, has not been studied by genetic means. Here, we show that Arabidopsis thaliana formin3 (AFH3) is an actin nucleation factor responsible for the formation of longitudinal actin cables in pollen tubes. The Arabidopsis AFH3 gene encodes a 785-amino acid polypeptide, which contains a formin homology 1 (FH1) and a FH2 domain. In vitro analysis revealed that the AFH3 FH1FH2 domains interact with the barbed end of actin filaments and have actin nucleation activity in the presence of G-actin or G actin-profilin. Overexpression of AFH3 in tobacco (Nicotiana tabacum) pollen tubes induced excessive actin cables, which extended into the tubes' apices.

To optimize fitness, plants must efficiently allocate their resources between growth and defense. Although phytohormone crosstalk has emerged as a major player in balancing growth and defense, the genetic basis by which plants manage this balance remains elusive. We previously identified a quantitative diseaseresistance locus, qRfg2, in maize (Zea mays) that protects against the fungal disease Gibberella stalk rot. Here, through map-based cloning, we demonstrate that the causal gene at qRfg2 is ZmAuxRP1, which encodes a plastid stroma-localized auxin-regulated protein. ZmAuxRP1 responded quickly to pathogen challenge with a rapid yet transient reduction in expression that led to arrested root growth but enhanced resistance to Gibberella stalk rot and Fusarium ear rot. ZmAuxRP1 was shown to promote the biosynthesis of indole-3-acetic acid (IAA), while suppressing the formation of benzoxazinoid defense compounds. ZmAuxRP1 presumably acts as a resource regulator modulating indole-3-glycerol phosphate and/or indole flux at the branch point between the IAA and benzoxazinoid biosynthetic pathways. The concerted interplay between IAA and benzoxazinoids can regulate the growth-defense balance in a timely and efficient manner to optimize plant fitness.

Sugarcane mosaic virus (SCMV) causes substantial losses of grain yield and forage biomass in susceptible maize worldwide. A major quantitative trait locus, Scmv1, has been identified to impart strong resistance to SCMV at the early infection stage. Here, we demonstrate that ZmTrxh, encoding an atypical h-type thioredoxin, is the causal gene at Scmv1, and that its transcript abundance correlated strongly with maize resistance to SCMV. ZmTrxh alleles, whether they are resistant or susceptible, share the identical coding/proximal promoter regions, but vary in the upstream regulatory regions. ZmTrxh lacks two canonical cysteines in the thioredoxin active-site motif and exists uniquely in the maize genome. Because of this, ZmTrxh is unable to reduce disulfide bridges but possesses a strong molecular chaperone-like activity. ZmTrxh is dispersed in maize cytoplasm to suppress SCMV viral RNA accumulation. Moreover, ZmTrxh-mediated maize resistance to SCMV showed no obvious correlation with the salicylic acid- and jasmonic acid-related defense signaling pathways. Taken together, our results indicate that ZmTrxh exhibits a distinct defense profile in maize resistance to SCMV, differing from previously characterized dominant or recessive potyvirus resistance genes.

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Tremendous progress has been made recently in understanding plant response to Fusarium graminearum infection. Here, the cytological aspect and molecular mechanism of maize defense to F. graminearum infection were characterized using a pair of near-isogenic lines (NIL), the resistant and the susceptible NIL. F. graminearum primarily penetrated the maize root tip and no penetration structure was found. The fungal biomass within the root correlated well with root-disease severity. Following inoculation, R-NIL and S-NIL plants significantly differed in percentage of diseased primary roots. In R-NIL roots, a fraction of exodermal cells collapsed to form cavities, and hyphae were confined to the outer exodermal cells. However, most exodermal cells shrank and turned brown, and fungi colonized the entire S-NIL root. In the R-NIL roots, the exodermal cells exhibited plasmolysis and atropous hyphal growth whereas, in the exodermal cells of the S-NIL roots, severe cellular degradation and membrane-coated, lushly grown hyphae were found. Transcriptome sequencing revealed comprehensive transcription reprogramming, reinforcement of a complex defense network, to enhance the systemic and basal resistance. This study reports a detailed microscopic analysis of F. graminearum infection on maize root, and provides insights into the molecular mechanisms underlying maize resistance to the pathogen.

BackgroundMaize rough dwarf disease (MRDD) is a devastating viral disease that results in considerable yield losses worldwide. Three major strains of virus cause MRDD, including maize rough dwarf virus in Europe, Mal de Río Cuarto virus in South America, and rice black-streaked dwarf virus in East Asia. These viral pathogens belong to the genus fijivirus in the family Reoviridae. Resistance against MRDD is a complex trait that involves a number of quantitative trait loci (QTL). The primary approach used to minimize yield losses from these viruses is to breed and deploy resistant maize hybrids.ResultsOf the 50 heterogeneous inbred families (HIFs), 24 showed consistent responses to MRDD across different years and locations, in which 9 were resistant and 15 were susceptible. We performed trait-marker association analysis on the 24 HIFs and found six chromosomal regions which were putatively associated with MRDD resistance. We then conducted QTL analysis and detected a major resistance QTL, qMrdd1, on chromosome 8. By applying recombinant-derived progeny testing to self-pollinated backcrossed families, we fine-mapped the qMrdd1 locus into a 1.2-Mb region flanked by markers M103-4 and M105-3. The qMrdd1 locus acted in a recessive manner to reduce the disease-severity index (DSI) by 24.2–39.3%. The genetic effect of qMrdd1 was validated using another F6 recombinant inbred line (RIL) population in which MRDD resistance was segregating and two genotypes at the qMrdd1 locus differed significantly in DSI values.ConclusionsThe qMrdd1 locus is a major resistance QTL, acting in a recessive manner to increase maize resistance to MRDD. We mapped qMrdd1 to a 1.2-Mb region, which will enable the introgression of qMrdd1-based resistance into elite maize hybrids and reduce MRDD-related crop losses.