ABSTRACT
Maize productivity is significantly impacted by drought; therefore, improvement of drought tolerance is a critical goal in maize breeding. To achieve this, a better understanding of the genetic basis of drought tolerance is necessary. Our study aimed to identify genomic regions associated with drought tolerance-related traits by phenotyping a mapping population of recombinant inbred lines (RILs) for two seasons under well-watered (WW) and water-deficit (WD) conditions. We also used single nucleotide polymorphism (SNP) genotyping through genotyping-by-sequencing to map these regions and attempted to identify candidate genes responsible for the observed phenotypic variation. Phenotyping of the RILs population revealed significant variability in most of the traits, with normal frequency distributions, indicating their polygenic nature. We generated a linkage map using 1,241 polymorphic SNPs distributed over 10 chromosomes (chrs), covering a total genetic distance of 5,471.55 cM. We identified 27 quantitative trait loci (QTLs) associated with various morphophysiological and yield-related traits, with 13 QTLs identified under WW conditions and 12 under WD conditions. We found one common major QTL (qCW2-1) for cob weight and a minor QTL (qCH1-1) for cob height that were consistently identified under both water regimes. We also detected one major and one minor QTL for the Normalized Difference Vegetation Index (NDVI) trait under WD conditions on chr 2, bin 2.10. Furthermore, we identified one major QTL (qCH1-2) and one minor QTL (qCH1-1) on chr 1 that were located at different genomic positions to those identified in earlier studies. We found co-localized QTLs for stomatal conductance and grain yield on chr 6 (qgs6-2 and qGY6-1), while co-localized QTLs for stomatal conductance and transpiration rate were identified on chr 7 (qgs7-1 and qTR7-1). We also attempted to identify the candidate genes responsible for the observed phenotypic variation; our analysis revealed that the major candidate genes associated with QTLs detected under water deficit conditions were related to growth and development, senescence, abscisic acid (ABA) signaling, signal transduction, and transporter activity in stress tolerance. The QTL regions identified in this study may be useful in designing markers that can be utilized in marker-assisted selection breeding. In addition, the putative candidate genes can be isolated and functionally characterized so that their role in imparting drought tolerance can be more fully understood.
ABSTRACT
Water deficit is a key limiting factor for maize (Zea mays L.) productivity. Elucidating the molecular regulatory networks of stress tolerance is crucial for genetic enhancement of drought tolerance. Two genotypes of maize contrasting in their yield response to water deficit were evaluated for tolerance traits of water relations, net CO2 assimilation rate, antioxidative metabolism and grain yield in relation to the expression levels, based on transcription profiling of genes involved in stress signaling, protein processing and energy metabolism to identify functional tolerance mechanisms. In the genotype SNJ201126 upregulation of calcium mediated signaling, plasma membrane and tonoplast intrinsic proteins and the membrane associated transporters contributed to better maintenance of water relations as evident from the higher relative water content and stomatal conductance at seedling and anthesis stages coupled with robust photosynthetic capacity and antioxidative metabolism. Further the protein folding machinery consisting of calnexin/calreticulin (CNX/CRT) cycle was significantly upregulated only in SNJ201126. While the down regulation of genes involved in photosystems and the enzymes of carbon fixation led to the relative susceptibility of genotype HKI161 in terms of reduced net CO2 assimilation rate, biomass and grain yield. Our results provide new insight into intrinsic functional mechanisms related to tolerance in maize. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12298-021-01003-4.
