Inheritance and molecular mapping of solitary/cluster fruit-bearing habit in Luffa.

Fruiting behaviour and sex form are important goals for Luffa breeders and this study aimed to shed light upon inheritance patterns for both these traits. The hermaphrodite form of Luffa acutangula (known as Satputia) is an underutilized vegetable with a unique clustered fruiting habit. Its desirable traits, such as plant architecture, earliness, as well as contrasting traits like unique clustered fruiting, bisexual flower, and crossability with Luffa acutangula (monoecious ridge gourd with solitary fruits), make it a potential source for trait improvement and mapping of desirable traits in Luffa. In the present study, we have elucidated the inheritance pattern of fruiting behaviour in Luffa using F2 mapping population generated from a cross between Pusa Nutan (Luffa acutangula, monoecious, solitary fruiting) × DSat-116 (Luffa acutangula, hermaphrodite, cluster fruiting). In F2 generation, the observed distribution of plant phenotypes fitted in the expected ratio of 3:1 (solitary vs cluster) for fruit-bearing habit. This is the first report of monogenic recessive control for cluster fruit-bearing habit in Luffa. Herein, we designate for the first time the gene symbol cl for cluster fruit bearing in Luffa. Linkage analysis revealed that SRAP marker ME10 EM4-280 was linked to the fruiting trait at the distance of 4.6 cM from the Cl locus. In addition, the inheritance pattern of hermaphrodite sex form in Luffa was also studied in the F2 population of Pusa Nutan × DSat-116 that segregated into 9:3:3:1 ratio (monoecious:andromonoecious:gynoecious:hermaphrodite), suggesting a digenic recessive control of hermaphrodite sex form in Luffa, which was further confirmed by the test cross. The inheritance and identification of molecular marker for cluster fruiting trait provides a basis for breeding in Luffa species.

Insight into a region of chickpea (Cicer arietinum L.) Chromosome 2 revealed potential candidate genes linked to Foc4 Fusarium wilt resistance.

Two markers on Chromosome 2 of chickpea (Cicer arietinum ) are reportedly associated with resistance to race 4 Fusarium wilt, and are frequently used in breeding. However, the genes in this region that actually confer wilt resistance are unknown. We aimed to characterise them using both in silico approaches and marker trait association (MTA) analysis. Of the 225 protein-encoding genes in this region, 51 showed significant differential expression in two contrasting chickpea genotypes under wilt, with potential involvement in stress response. From a diverse set of 244 chickpea genotypes, two sets of 40 resistant and 40 susceptible genotypes were selected based on disease incidence and amplification pattern of the TA59 marker. All cultivars were further genotyped with 1238 single nucleotide polymorphisms (SNPs) specific to the 51 genes; only seven SNPs were significantly correlated with disease. SNP Ca2_24099002, specific to the LOC101498008 (Transmembrane protein 87A) gene, accounted for the highest phenotypic variance for disease incidence at 16.30%, whereas SNPs Ca2_25166118 and Ca2_27029215, specific to the LOC101494644 (ß-glucosidase BoGH3B-like) and LOC101505289 (Putative tRNA pseudouridine synthase) genes, explained 10.51% and 10.50% of the variation, respectively, in the sets with contrasting disease susceptibility. Together with the TA59 and TR19 markers, these SNPs can be used in a chickpea breeding scheme to develop wilt resistance.

Shoot transcriptome revealed widespread differential expression and potential molecular mechanisms of chickpea (Cicer arietinum L.) against Fusarium wilt.

Introduction: The yield of chickpea is severely hampered by infection wilt caused by several races of Fusarium oxysporum f. sp. ciceris (Foc). Methods: To understand the underlying molecular mechanisms of resistance against Foc4 Fusarium wilt, RNA sequencing-based shoot transcriptome data of two contrasting chickpea genotypes, namely KWR 108 (resistant) and GL 13001 (susceptible), were generated and analyzed. Results and Discussion: The shoot transcriptome data showed 1,103 and 1,221 significant DEGs in chickpea genotypes KWR 108 and GL 13001, respectively. Among these, 495 and 608 genes were significantly down and up-regulated in genotypes KWR 108, and 427 and 794 genes were significantly down and up-regulated in genotype GL 13001. The gene ontology (GO) analysis of significant DEGs was performed and the GO of the top 50 DEGs in two contrasting chickpea genotypes showed the highest cellular components as membrane and nucleus, and molecular functions including nucleotide binding, metal ion binding, transferase, kinase, and oxidoreductase activity involved in biological processes such as phosphorylation, oxidation-reduction, cell redox homeostasis process, and DNA repair. Compared to the susceptible genotype which showed significant up-regulation of genes involved in processes like DNA repair, the significantly up-regulated DEGs of the resistant genotypes were involved in processes like energy metabolism and environmental adaptation, particularly host-pathogen interaction. This indicates an efficient utilization of environmental adaptation pathways, energy homeostasis, and stable DNA molecules as the strategy to cope with Fusarium wilt infection in chickpea. The findings of the study will be useful in targeting the genes in designing gene-based markers for association mapping with the traits of interest in chickpea under Fusarium wilt which could be efficiently utilized in marker-assisted breeding of chickpea, particularly against Foc4 Fusarium wilt.