Quantitative Population Epigenetics in Screening and Development of Regulator-Active Factors of the Farming System

Likewise, index selection based on statistical genetic theory in plant and animal breeding the methodology "Quantitative Population Epigenetics" can be appropriated to improve efficiency in screening and development of regulator-active factors of the farming system for potential to enhance quantitative characters such as yield, standability and resistance to unfavorable environmental influences (e.g., water stress, cold temperatures, disease resistance). For example, as was shown for an effect of monoethanolamine on yield and water use efficiency of spring barley plants (Bergmann et al. 1991)

Sustainable deployment of QTLs conferring quantitative resistance to crops: first lessons from a stochastic model

Quantitative plant disease resistance is believed to be more durable than qualitative resistance, since it exerts less selective pressure on the pathogens. However, the process of progressive pathogen adaptation to quantitative resistance is poorly understood, which makes it difficult to predict its durability or to derive principles for its sustainable deployment. Here, we study the dynamics of pathogen adaptation in response to quantitative plant resistance affecting pathogen reproduction rate and its carrying capacity. We developed a stochastic model for the continuous evolution of a pathogen population within a quantitatively resistant host. We assumed that pathogen can adapt to a host by the progressive restoration of reproduction rate or of carrying capacity, or of both. Our model suggests that a combination of QTLs affecting distinct pathogen traits was more durable if the evolution of repressed traits was antagonistic. Otherwise, quantitative resistance that depressed only pathogen reproduction was more durable. In order to decelerate the progressive pathogen adaptation, QTLs that decrease the pathogen's ability to extend must be combined with QTLs that decrease the spore production per lesion or the infection efficiency or that increase the latent period. Our theoretical framework can help breeders to develop principles for sustainable deployment of quantitative trait loci.

Quantitative trait loci mapping for resistance to maize streak virus in F2: 3 population of tropical maize

Open Access Article; Published online: 01 Feb 2020Maize streak virus (MSV) continues to be a major biotic constraint for maize production throughout Africa. Concerning the quantitative nature of inheritance of resistance to MSV disease (MSVD), we sought to identify new loci for MSV resistance in maize using F2:3 population. The mapping population was artificially inoculated with viruliferous leafhoppers under screenhouse and evaluated for MSVD resistance. Using 948 DArT markers, we identified 18 quantitative trait loci (QTLs) associated with different components of MSVD resistance accounting for 3.1–21.4% of the phenotypic variance, suggesting that a total of eleven genomic regions covering chromosomes 1, 2, 3, 4, 5 and 7 are probably required for MSVD resistance. Two new genomic regions on chromosome 4 revealed the occurrence of co-localized QTLs for different parameters associated with MSVD resistance. Moreover, the consistent appearance of QTL on chromosome 7 for MSVD resistance is illustrating the need for fine-mapping of this locus. In conclusion, these QTLs could provide additional source for breeders to develop MSV resistance

Genomic analysis of quantitative disease resistance during maize-hemibiotrophic leaf blight pathogen interaction

Plant diseases account for more than 40% of crop losses. Breeding for disease resistance is the most effective means of crop protection against these losses. Disease resistance in plants is categorized into qualitative and quantitative resistance. Qualitative disease resistance is controlled by single major genes that confer complete or near complete resistance against disease pathogens. However, the absence or instability of qualitative resistance in many crop-pathogen interaction systems has necessitated a shift in research toward quantitative disease resistance (QDR). QDR is conditioned by several genes of minor effects resulting in reduced levels of disease. The multigenic nature of QDR overcomes the limitations of qualitative disease resistance. As a fairly new field of research, the specific mechanisms underlying the genetic architecture of QDR in response to pathogen attack are still not well understood. The goal of this research was to identify and characterize the genetic, molecular and mechanistic bases of QDR in maize against hemi-biotrophic Setosphaeria turcica, the causative agent of Northern leaf blight (NLB). The unique lifestyle of Setosphaeria turcica, as well as the sequenced and annotated maize genome provide an opportunity to study the quantitative nature of host-hemi-biotrophic interactions. This research employed both phenotypic and genetic approaches to elucidate the mechanisms that underlie QDR with the aim of improving plant health and production. A new genetic map for the Intermated B73 x Mo17 Syn10 doubled haploid line (IBMSyn10DHL) population was created and evaluated. To identify and characterize the genetic basis of quantitative disease resistance in maize-S. turcica interaction, IBMDHLs were tested against two isolates of Setosphaeria turcica across multiple environments. Unique and overlapping NLB resistance-related QTL were identified within and across environments respectively. Additionally, IBMDHL and their backcross hybrid populations were tested in Iowa against Iowa NLB isolate to estimate the genetic mode of action of loci underlying quantitative disease resistance. Results from this research highlighted the multigenic nature and specificity of QDR and the genetic effects of genes underlying QDR. Furthermore, previously reported and novel disease resistance-related QTL were identified

Recent Developments in Genomic Selection for Minor Gene Quantitative Disease Resistance Plant Breeding

To speed up the development of improved crop varieties, genomics assisted plant breeding is becoming an important tool. With traditional breeding and marker assisted selection, there have been several achievements in breeding for diseases resistance. Most research for disease resistance has been focused on major disease resistance genes which are highly effective although very vulnerable to breakdown with rapid changes in pathogenic races. In contrast, breeding for minor gene quantitative resistance can produce more durable plant varieties although it is very slow and challenging breeding. As the genetic architecture of the plant disease resistance shifts from single major R genes to many minor quantitative genes, the most appropriate approach for molecular plant breeding is genomic selection (GS) than marker assisted selection or conventional breeding. With the advent of new genomic tools, GS has emerged as one of the most important approaches for predicting genotype performance to improve genetically complex quantitative traits. Consequently, GS helps to accelerate the rate of genetic gain in breeding by using whole genome sequence data to predict the breeding value of offspring. GS breeding for quantitative resistance will therefore necessitate whole genome prediction models and selection methodology as implemented for classical complex traits. With the implementation of GS for yield and other economically important traits, whole genome marker profiles are available for the entire set of breeding lines, enabling genomic selection for disease resistance with no additional direct cost. Therefore, recent developments in GS including a two stream GS + de novo GWAS models (GS+) and GS for combined highest level of quantitative resistance with R genes (QR +R gene) individuals are expected to further advance disease resistance plant breeding and briefly discussed

The phenotypic expression of QTLs for partial resistance to barley leaf rust during plant development

Partial resistance is generally considered to be a durable form of resistance. In barley, Rphq2, Rphq3 and Rphq4 have been identified as consistent quantitative trait loci (QTLs) for partial resistance to the barley leaf rust pathogen Puccinia hordei. These QTLs have been incorporated separately into the susceptible L94 and the partially resistant Vada barley genetic backgrounds to obtain two sets of near isogenic lines (NILs). Previous studies have shown that these QTLs are not effective at conferring disease resistance in all stages of plant development. In the present study, the two sets of QTL–NILs and the two recurrent parents, L94 and Vada, were evaluated for resistance to P. hordei isolate 1.2.1 simultaneously under greenhouse conditions from the first leaf to the flag leaf stage. Effect of the QTLs on resistance was measured by development rate of the pathogen, expressed as latency period (LP). The data show that Rphq2 prolongs LP at the seedling stage (the first and second leaf stages) but has almost no effect on disease resistance in adult plants. Rphq4 showed no effect on LP until the third leaf stage, whereas Rphq3 is consistently effective at prolonging LP from the first leaf to the flag leaf. The changes in the effectiveness of Rphq2 and Rphq4 happen at the barley tillering stage (the third to fourth leaf stages). These results indicate that multiple disease evaluations of a single plant by repeated inoculations of the fourth leaf to the flag leaf should be conducted to precisely estimate the effect of Rphq4. The present study confirms and describes in detail the plant development-dependent effectiveness of partial resistance genes and, consequently, will enable a more precise evaluation of partial resistance regulation during barley developmen

Mapping spot blotch & common root rot (causal agent: bipolaris sorokiniana) resistance genes in barley

The fungal pathogen Bipolaris sorokiniana (teleomorph Cochliobolus sativus)causes the foliar disease spot blotch (SB) and the root disease common root rot (CRR). Spot blotch and CRR are serious disease constraints to barley production in warmer growing regions of the world, with estimated yield losses ranging from 30-70% from SB and 15-30% for CRR. Although chemical treatments may assist in controlling spot blotch infections, the most effective and environmentally sound means of control for each disease is breeding for varieties with natural resistance. In Australia, no commercially available varieties offer resistance to either SB or CRR. This study has sought to establish molecular markers that will be useful for selecting for resistance to each of these important fungal diseases. Barley cultivars derived from the breeding line NDB112 have provided durable SB resistance in the North Dakota region of the USA for over 40 years. The robustness of this resistance had not been determined under Australian environmental conditions or with those B. sorokiniana pathotypes present within Australia. To elucidate the genetics of resistance, two seedling and two field trials were conducted on an ND11231-12/VB9524 (ND/VB) doubled haploid (DH) population (180 lines). A molecular map of the ND/VB population was curated in order to provide a firm basis for mapping of resistance loci. Composite interval mapping revealed that different gene combinations are effective at different stages of plant development. Seedling resistance was found to be conditioned by a major locus on the short arm of chromosome 7H and this region was validated in the related population ND11231-11/WI2875*17. A minor quantitative locus on chromosome 5HS was detected in one of the two seedling trials. However, this region requires further investigation to confirm its association to SB resistance in this population. Field resistance to SB in adult plants was found to be associated with two major quantitative trait loci (QTL)on chromosomes 7HS and 3HS; and a putative third minor QTL on chromosome 2HS. The 7H region is common between seedling and field resistance and is the most important locus for the expression of resistance at both stages of plant development. These findings largely concur with genetic studies of this trait in tworowed barley germplasm in North American environments. Common root rot is a difficult disease to phenotype for, and breeding programs will benefit from the identification of molecular markers linked to resistance. Data was provided from field trials of subsets of the population over four years. Using a novel approach combining the efficiency of bulked-segregant analysis with highthroughput Diversity Arrays Technology markers (BSA-DArT), CRR resistance was found to be conditioned by three putative QTL in an unmapped Delta/Lindwall population. QTL were identified on chromosomes 2HS, 4HS, and 7HS. To validate the trait-linkage associations between the DArT markers and the CRR QTL,microsatellite (SSR) markers known to map to the regions identified by BSA-DArT were used. The 2H and 4H regions were validated using marker regression of the SSR markers in most seedling trials, whereas the 7H QTL, which is proximal to the location of the SB resistance QTL in the ND/VB population, was detected in only one seedling trial. The QTL identified in this study offer potential to combat the foliar and root diseases causes by this fungal pathogen. The chromosomal location of QTL for SB and CRR resistance have been found to differ in the ND/VB and D/L populations,which suggests that resistance to each disease is independently inherited. Further research is required to confirm the hypothesis that it is possible to combine resistance to both diseases into a single genotype. Such allelic combinations would provide elite germplasm that would benefit barley breeding programs world-wide