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Background Pod shatter resistance is an important trait in Brassica species, significantly impacting the yield and profitability of growers. Identifying genomic regions and understanding genes underlying shatter resistance is a major objective of breeding programs. Brassica rapa , commonly known as rape or field mustard, is an ancestral species of Brassica napus and Brassica juncea – the most widely oilseed crops grown worldwide. In this study, we performed diversity analysis of B. rapa accessions, bulked segregant analysis based quantitative trait locus-sequencing (QTL-seq), and traditional quantitative trait locus (QTL) mapping in an F 2 population to identify genomic regions associated with pod shatter resistance in B. rapa . Results A considerable genetic variation for pod shatter resistance, measured as rupture energy (RE), varied from 0.63 to 3.49 mJ (½) was revealed among 90 accessions of B. rapa . Cluster analysis based on 10,324 DArTseq markers showed that pod shatter-resistant accessions originated from diverse sources. We further investigated the genetic and anatomical bases of variation in pod shatter resistance from two contrasting parental lines, ATC90153 (maternal parent with high RE) and ATC91215 (paternal parent with low RE). Bulked segregant resequencing analysis of parental lines and two pooled samples, prepared from 10 resistant and 10 sensitive lines to pod shatter, identified three genomic regions for shatter resistance on chromosomes A06 and A09. Traditional QTL analysis validated marker-pod shatter resistance associations on chromosomes A06 and A09 in the same F 2 population using a linkage map based on 23,274 DArTseq markers. Physical positions of significantly associated markers and the priori pod dehiscence genes on the B. rapa reference genome sequence suggested BEE1/PEROXIDASE/TCP8 on A06 and ADPG1/SHP1/MYB116 genes on A09 as potential candidates for pod shatter resistance. Sequence comparison of parental lines identified sequence variants (194 SNPs and 74 InDELs on A06, and two SNPs and two InDELs on A09) in the promoter and downstream regions of B. rapa genes within the QTL. Conclusions We identified QTLs and priori candidate genes associated with variation in pod shatter resistance on chromosomes A06 and A09 in B. rapa . This study provides potential gene targets to understand molecular mechanisms and improve pod shatter resistance in Brassica crops.

Background Transition to flowering at the right time is critical for local adaptation and to maximize grain yield in crops. Canola is an important oilseed crop with extensive variation in flowering time among varieties. However, our understanding of underlying genes and their role in canola productivity is limited. Results We report our analyses of a diverse GWAS panel (300–368 accessions) of canola and identify SNPs that are significantly associated with variation in flowering time and response to photoperiod across multiple locations. We show that several of these associations map in the vicinity of FLOWERING LOCUS T ( FT ) paralogs and its known transcriptional regulators. Complementary QTL and eQTL mapping studies, conducted in an Australian doubled haploid population, also detected consistent genomic regions close to the FT paralogs associated with flowering time and yield-related traits. FT sequences vary between accessions. Expression levels of FT in plants grown in field (or under controlled environment cabinets) correlated with flowering time. We show that markers linked to the FT paralogs display association with variation in multiple traits including flowering time, plant emergence, shoot biomass and grain yield. Conclusions Our findings suggest that FT paralogs not only control flowering time but also modulate yield-related productivity traits in canola.

Resistance to pod shattering (shatter resistance) is a target trait for global rapeseed (canola, Brassica napus L.), improvement programs to minimise grain loss in the mature standing crop, and during windrowing and mechanical harvest. We describe the genetic basis of natural variation for shatter resistance in B. napus and show that several quantitative trait loci (QTL) control this trait. To identify loci underlying shatter resistance, we used a novel genotyping-by-sequencing approach DArT-Seq. QTL analysis detected a total of 12 significant QTL on chromosomes A03, A07, A09, C03, C04, C06, and C08; which jointly account for approximately 57% of the genotypic variation in shatter resistance. Through Genome-Wide Association Studies, we show that a large number of loci, including those that are involved in shattering in Arabidopsis, account for variation in shatter resistance in diverse B. napus germplasm. Our results indicate that genetic diversity for shatter resistance genes in B. napus is limited; many of the genes that might control this trait were not included during the natural creation of this species, or were not retained during the domestication and selection process. We speculate that valuable diversity for this trait was lost during the natural creation of B. napus. To improve shatter resistance, breeders will need to target the introduction of useful alleles especially from genotypes of other related species of Brassica, such as those that we have identified.

Sustainable canola production is essential to meet growing human demands for vegetable oil, biodiesel, and meal for stock feed markets. Blackleg, caused by the fungal pathogen, Leptosphaeria maculans is a devastating disease that can lead to significant yield loss in many canola production regions worldwide. Breakdown of race-specific resistance to L. maculans in commercial cultivars poses a constant threat to the canola industry. To identify new alleles, especially for quantitative resistance (QR), we analyzed 177 doubled haploid (DH) lines derived from an RP04/Ag-Outback cross. DH lines were evaluated for QR under field conditions in three experiments conducted at Wagga Wagga (2013, 2014) and Lake Green (2015), and under shade house conditions using the ‘ascospore shower’ test. DH lines were also characterized for qualitative R gene-mediated resistance via cotyledon tests with two differential single spore isolates, IBCN17 and IBCN76, under glasshouse conditions. Based on 18,851 DArTseq markers, a linkage map representing 2,019 unique marker bins was constructed and then utilized for QTL detection. Marker regression analysis identified 22 significant marker associations for resistance, allowing identification of two race-specific resistance R genes, Rlm3 and Rlm4 , and 21 marker associations for QR loci. At least three SNP associations for QR were repeatedly detected on chromosomes A03, A07 and C04 across phenotyping environments. Physical mapping of markers linked with these consistent QR loci on the B. napus genome assembly revealed their localization in close proximity of the candidate genes of B. napus BnaA03g26760D (A03), BnaA07g20240D (A07) and BnaC04g02040D (C04). Annotation of these candidate genes revealed their association with protein kinase and jumonji proteins implicated in defense resistance. Both Rlm3 and Rlm4 genes identified in this DH population did not show any association with resistance loci detected under either field and/or shade house conditions (ascospore shower) suggesting that both genes are ineffective in conferring resistance to L. maculans in Australian field conditions. Taken together, our study identified sequence-based molecular markers for dissecting R and QR loci to L. maculans in a canola DH population from the RP04/Ag-Outback cross.

Canola exhibits an extensive genetic variation for resistance to blackleg disease, caused by the fungal pathogen Leptosphaeria maculans . Despite the identification of several Avr effectors and R (race-specific) genes, specific interactions between Avr-R genes are not yet fully understood in the Brassica napus–L. maculans pathosystem. In this study, we investigated the genetic basis of resistance in an F 2 : 3 population derived from Australian canola varieties CB-Telfer ( Rlm4 )/ATR-Cobbler ( Rlm4 ) using a single-spore isolate of L. maculans , PHW1223. A genetic linkage map of the CB-Telfer/ATR-Cobbler population was constructed using 7,932 genotyping-by-sequencing-based DArTseq markers and subsequently utilized for linkage and haplotype analyses. Genetic linkage between DArTseq markers and resistance to PHW1223 isolate was also validated using the B. napus 60K Illumina Infinium array. Our results revealed that a major locus for resistance, designated as Rlm13 , maps on chromosome C03. To date, no R gene for resistance to blackleg has been reported on the C subgenome in B. napus . Twenty-four candidate R genes were predicted to reside within the quantitative trait locus (QTL) region. We further resequenced both the parental lines of the mapping population (CB-Telfer and ATR-Cobbler, > 80 × coverage) and identified several structural sequence variants in the form of single-nucleotide polymorphisms (SNPs), insertions/deletions (InDels), and presence/absence variations (PAVs) near Rlm13 . Comparative mapping revealed that Rlm13 is located within the homoeologous A03/C03 region in ancestral karyotype block “R” of Brassicaceae . Our results provide a “target” for further understanding the Avr–Rlm13 gene interaction as well as a valuable tool for increasing resistance to blackleg in canola germplasm.

Background Understanding the genetic control of pod shatter resistance and its association with pod length is crucial for breeding improved pod shatter resistance and reducing pre-harvest yield losses due to extensive shattering in cultivars of Brassica species . In this study, we evaluated a doubled haploid (DH) mapping population derived from an F 1 cross between two Brassica carinata parental lines Y-BcDH64 and W-BcDH76 (YWDH), originating from Ethiopia and determined genetic bases of variation in pod length and pod shatter resistance, measured as rupture energy. The YWDH population, its parental lines and 11 controls were grown across three years for genetic analysis. Results By using three quantitative trait loci (QTL) analytic approaches, we identified nine genomic regions on B02, B03, B04, B06, B07 and C01 chromosomes for rupture energy that were repeatedly detected across three growing environments. One of the QTL on chromosome B07, flanked with DArTseq markers 100,046,735 and 100,022,658, accounted for up to 27.6% of genetic variance in rupture energy. We observed no relationship between pod length and rupture energy, suggesting that pod length does not contribute to variation in pod shatter resistance. Comparative mapping identified six candidate genes; SHP1 on B6 , FUL and MAN on chromosomes B07, IND and NST2 on B08, and MAN7 on C07 that mapped within 0.2 Mb from the QTL for rupture energy. Conclusion The results suggest that favourable alleles of stable QTL on B06, B07, B08 and C01 for pod shatter resistance can be incorporated into the shatter-prone B. carinata and its related species to improve final seed yield at harvest.

Pod shatter is a trait of agricultural relevance that ensures plants dehisce seeds in their native environment and has been subjected to domestication and selection for non-shattering types in several broadacre crops. However, pod shattering causes a significant yield reduction in canola ( Brassica napus L.) crops. An interspecific breeding line BC95042 derived from a B. rapa/B. napus cross showed improved pod shatter resistance (up to 12-fold than a shatter-prone B. napus variety). To uncover the genetic basis and improve pod shatter resistance in new varieties, we analysed F 2 and F 2:3 derived populations from the cross between BC95042 and an advanced breeding line, BC95041, and genotyped with 15,498 DArTseq markers. Through genome scan, interval and inclusive composite interval mapping analyses, we identified seven quantitative trait loci (QTLs) associated with pod rupture energy, a measure for pod shatter resistance or pod strength, and they locate on A02, A03, A05, A09 and C01 chromosomes. Both parental lines contributed alleles for pod shatter resistance. We identified five pairs of significant epistatic QTLs for additive x additive, additive dominance and dominance x dominance interactions between A01/C01, A03/A07, A07/C03, A03/C03, and C01/C02 chromosomes for rupture energy. QTL effects on A03/A07 and A01/C01 were in the repulsion phase. Comparative mapping identified several candidate genes ( AG , ABI3 , ARF3 , BP1 , CEL6 , FIL, FUL , GA2OX2 , IND , LATE , LEUNIG , MAGL15 , RPL , QRT2 , RGA , SPT and TCP10 ) underlying main QTL and epistatic QTL interactions for pod shatter resistance. Three QTLs detected on A02, A03, and A09 were near the FUL (FRUITFULL) homologues BnaA03g39820D and BnaA09g05500D . Focusing on the FUL , we investigated putative motifs, sequence variants and the evolutionary rate of its homologues in 373 resequenced B. napus accessions of interest. BnaA09g05500D is subjected to purifying selection as it had a low Ka/Ks ratio compared to other FUL homologues in B. napus. This study provides a valuable resource for genetic improvement for yield through an understanding of the genetic mechanism controlling pod shatter resistance in Brassica species.

Seed lost due to easy pod dehiscence at maturity (pod shatter) is a major problem in several members of Brassicaceae family. We investigated the level of pod shatter resistance in Ethiopian mustard ( ) and identified quantitative trait loci (QTL) for targeted introgression of this trait in Ethiopian mustard and its close relatives of the genus . A set of 83 accessions of , collected from the Australian Grains Genebank, was evaluated for pod shatter resistance based on pod rupture energy (RE). In comparison to (RE = 2.16 mJ), accessions had higher RE values (2.53 to 20.82 mJ). A genetic linkage map of an F population from two contrasting selections, BC73526 (shatter resistant with high RE) and BC73524 (shatter prone with low RE) comprising 300 individuals, was constructed using a set of 6,464 high quality DArTseq markers and subsequently used for QTL analysis. Genetic analysis of the F and F derived lines revealed five statistically significant QTL (LOD ≥ 3) that are linked with pod shatter resistance on chromosomes B1, B3, B8, and C5. Herein, we report for the first time, identification of genetic loci associated with pod shatter resistance in . These characterized accessions would be useful in breeding programs for introgression of pod shatter resistance alleles in to elite breeding lines. Molecular markers would assist marker-assisted selection for tracing the introgression of resistant alleles. Our results suggest that the value of the germplasm collections can be harnessed through genetic and genomics tools.

The first confirmed mechanism for aluminum (Al) resistance in plants is encoded by the wheat (Triticum aestivum) gene, TaALMT1, on chromosome 4DL. TaALMT1 controls the Al-activated efflux of malate from roots, and this mechanism is widespread among Al-resistant genotypes of diverse genetic origins. This study describes a second mechanism for Al resistance in wheat that relies on citrate efflux. Citrate efflux occurred constitutively from the roots of Brazilian cultivars Carazinho, Maringa, Toropi, and Trintecinco. Examination of two populations segregating for this trait showed that citrate efflux was controlled by a single locus. Whole-genome linkage mapping using an F₂ population derived from a cross between Carazinho (citrate efflux) and the cultivar EGA-Burke (no citrate efflux) identified a major locus on chromosome 4BL, Xcec, which accounts for more than 50% of the phenotypic variation in citrate efflux. Mendelizing the quantitative variation in citrate efflux into qualitative data, the Xcec locus was mapped within 6.3 cM of the microsatellite marker Xgwm495 locus. This linkage was validated in a second population of F₂:₃ families derived from a cross between Carazinho and the cultivar Egret (no citrate efflux). We show that expression of an expressed sequence tag, belonging to the multidrug and toxin efflux (MATE) gene family, correlates with the citrate efflux phenotype. This study provides genetic and physiological evidence that citrate efflux is a second mechanism for Al resistance in wheat.