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Background: Optimization of shade avoidance response (SAR) is crucial for enhancing crop yield in high-density planting conditions in modern agriculture, but a comprehensive study of the regulatory network of SAR is still lacking in monocot crops. Results: In this study, the genome-wide early responses in maize seedlings to the simulated shade (low red/far-red ratio) and also to far-red light treatment were transcriptionally profiled. The two processes were predominantly mediated by phytochrome B and phytochrome A, respectively. Clustering of differentially transcribed genes (DTGs) along with functional enrichment analysis identified important biological processes regulated in response to both treatments. Co-expression network analysis identified two transcription factor modules as potentially pivotal regulators of SAR and de-etiolation, respectively. A comprehensive cross-species comparison of orthologous DTG pairs between maize and Arabidopsis in SAR was also conducted, with emphasis on regulatory circuits controlling accelerated flowering and elongated growth, two physiological hallmarks of SAR. Moreover, it was found that the genome-wide distribution of DTGs in SAR and de-etiolation both biased toward the maize1 subgenome, and this was associated with differential retention of various cis-elements between the two subgenomes. Conclusions: The results provide the first transcriptional picture for the early dynamics of maize phytochrome signaling. Candidate genes with regulatory functions involved in maize shade avoidance response have been identified, offering a starting point for further functional genomics investigation of maize adaptation to heavily shaded field conditions. [ABSTRACT FROM AUTHOR]

Background Understanding genetic control of tassel and ear architecture in maize (Zea mays L. ssp. mays) is important due to their relationship with grain yield. High resolution QTL mapping is critical for understanding the underlying molecular basis of phenotypic variation. Advanced populations, such as recombinant inbred lines, have been broadly adopted for QTL mapping; however, construction of large advanced generation crop populations is time-consuming and costly. The rapidly declining cost of genotyping due to recent advances in next-generation sequencing technologies has generated new possibilities for QTL mapping using large early generation populations. Results A set of 708 F2 progeny derived from inbreds Chang7-2 and 787 were generated and genotyped by whole genome low-coverage genotyping-by-sequencing methods (average 0.04×). A genetic map containing 6,533 bin-markers was constructed based on the parental SNPs and a sliding-window method, spanning a total genetic distance of 1,396 cM. The high quality and accuracy of this map was validated by the identification of two well-studied genes, r1, a qualitative trait locus for color of silk (chromosome 10) and ba1 for tassel branch number (chromosome 3). Three traits of tassel and ear architecture were evaluated in this population, a total of 10 QTL were detected using a permutation-based-significance threshold, seven of which overlapped with reported QTL. Three genes (GRMZM2G316366, GRMZM2G492156 and GRMZM5G805008) encoding MADS-box domain proteins and a BTB/POZ domain protein were located in the small intervals of qTBN5 and qTBN7 (∼800 Kb and 1.6 Mb in length, respectively) and may be involved in patterning of tassel architecture. The small physical intervals of most QTL indicate high-resolution mapping is obtainable with this method. Conclusions We constructed an ultra-high-dentisy linkage map for the large early generation population in maize. Our study provides an efficient approach for fast detection of quantitative loci responsible for complex trait variation with high accuracy, thus helping to dissect the underlying molecular basis of phenotypic variation and accelerate improvement of crop breeding in a cost-effective fashion. [ABSTRACT FROM AUTHOR]

Background: Maize 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. Results: Of 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. Conclusions: The 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. [ABSTRACT FROM AUTHOR]