Factors contributing to variation in heading date in spring barley were examined in several studies commencing with a survey of developmental variation in a large collection of genotypes and concluding with the molecular genetic analysis of 7 doubled haploid populations. Genotypes varied considerably in their specific responses to photoperiod and vernalisation, and in the duration of a pre-inductive (or juvenile) phase defined in this paper as a 'basic vegetative period'. The latter includes differential genotype responses to ambient temperature and their interaction with photoperiod. Combinations of these largely independent environmental variables account for variation in heading date associated with differences in growing season conditions, particularly geographic region, sowing dates, and cultivar adaptation. Under extended and natural (short) photoperiods, in both summer and winter field plantings, conventional genetic analysis was characterised by simple Mendelian segregation combined with considerable transgressive segregation within distinct early and late flowering subpopulations. Equivalent transgressive segregation characterised molecular genetic analysis that identified 16 quantitative trait loci (QTLs) with contributions ranging from >50% of the variation recorded to <10%. These were dominated by 2 QTLs located on chromosome 2, one of which on 2HS was associated with response to extended photoperiod and the other, located near the centromere, with variation in the duration of the basic vegetative period. As only one population segregated for response to vernalisation, all analyses were restricted to parents and progeny homozygous for no response. Three other QTLs on 1HL, 3HL, and 5HL were primarily associated with vernalised parents and progeny characterised by prostrate seedling growth habits, which questions any assumption of a pleiotrophic association between genes for vernalisation and growth habit.The potential for exploiting markers for selection is considered to be limited by the considerable transgressive segregation observed in lines homozygous for parental alleles, and the limited understanding of the causes of variation in the phenotypic expression of the QTLs identified. Such markers would be useful in the selection of backcrossed progeny and in developing materials for investigating fundamental mechanisms contributing to developmental variation.

Barley seed dormancy is controlled by multiple genes that have a strong interaction with the environment. Lack of adequate dormancy results in pre-harvest sprouting in the field under wet weather conditions. On the other hand, too much dormancy has a detrimental effect in the malting house. There is only a very 'narrow window' of dormancy for malting barley. Harrington barley, which has been a dominant malting variety in the international market and widely used in Australia barley breeding programs, is highly susceptible to pre-harvest sprouting. A doubled haploid (DH) population derived from a cross of Chebec/Harrington was used to search for molecular markers linked with seed dormancy and pre-harvest sprouting. One major quantitative trait locus (QTL) was identified to control pre-harvest sprouting measured by α-amylase activity in barley grains, and could explain >70% of the phenotypic variation. This QTL was located on chromosome 5HL and flanked by restriction fragment length polymorphism (RFLP) marker CDO506 and simple sequence repeat (SSR) marker GMS1. The SSR marker (GMS1) linked with this QTL was further validated in a Stirling/Harrington DH population. A minor QTL on chromosome 2H accounted for 8% of phenotypic variation. Two QTLs for seed dormancy were located on chromosomes 2H and 5HL. The major QTL for dormancy coincided with the QTL for pre-harvest sprouting at chromosome 5HL and explained 61% of phenotypic variation. Since the presence of the Harrington allele at this locus favoured not only pre-harvest sprouting, but also increased malting extract, diastatic power, α-amylase, and free amino acid nitrogen, development of high malting quality varieties with pre-harvest sprouting tolerance would appear to be difficult.

Abstract. Barley kernel discoloration (KD) leads to substantial annual loss in value through downgrading and discounting of malting barley. KD is a difficult trait to introgress into elite varieties as it is controlled by multiple genes and strongly influenced by environment and maturity. As the first step towards marker assisted selection for KD tolerance, we mapped quantitative trait loci (QTLs) controlling KD measured by grain brightness [Minolta L; (Min L)], redness (Min a), and yellowness (Min b) in 7 barley populations. One to 3 QTLs were detected for grain brightness in various populations, and one QTL could account for 5-31% of the phenotypic variation. The QTL located around the centromere region of chromosome 2H was consistently detected in 6 of the 7 populations, explaining up to 28% of the phenotypic variation. In addition, QTLs for grain brightness were most frequently identified on chromosomes 3H and 7H in various populations. Australian varieties Galleon, Chebec, and Sloop contribute an allele to increase grain brightness on chromosome 7H in 3 different populations. A major gene effect was detected for grain redness. One QTL on chromosome 4H explained 54% of the phenotypic variation in the Sloop/Halcyon population, and was associated with the blue aleurone trait. A second QTL was detected on the long arm of chromosome 2H in 3 populations, accounting for 23-47% of the phenotypic variation. The major QTLs for grain yellowness were mapped on chromosomes 2H and 5H. There were strong associations between the QTLs for heading date, grain brightness, and yellowness. The molecular markers linked with the major QTLs should be useful for marker assisted selection for KD.

Chickpea production is constrained worldwide by the necrotrophic fungal pathogen Ascochyta rabiei, the causal agent of ascochyta blight (AB). In order to reduce the impact of this disease, novel sources of resistance are required in chickpea cultivars. Here, we screened a new collection of wild Cicer accessions for AB resistance and identified accessions resistant to multiple, highly pathogenic isolates. In addition to this, analyses demonstrated that some collection sites of Cicer echinospermum harbour predominantly resistant accessions, knowledge that can inform future collection missions. Furthermore, a genome-wide association study identified regions of the Cicer reticulatum genome associated with AB resistance and investigation of these regions identified candidate resistance genes. Taken together, these results can be utilised to enhance the resistance of chickpea cultivars to this globally yield-limiting disease.

The plant immune system is made up of a complex response network that involves several lines of defense to fight invading pathogens. Fungal plant pathogens on the other hand, have evolved a range of ways to infect their host. The interaction between Ascochyta lentis and two lentil genotypes was explored to investigate the progression of ascochyta blight (AB) in lentils. In this study, we developed an Agrobacterium tumefaciens-mediated transformation system for A. lentis by constructing a new binary vector, pATMT-GpdGFP, for the constitutive expression of green fluorescent protein (EGFP). Green fluorescence was used as a highly efficient vital marker to study the developmental changes in A. lentis during AB disease progression on the susceptible and resistant lentil accessions, ILL6002 and ILL7537, respectively. The initial infection stages were similar in both the resistant and susceptible accessions where A. lentis uses infection structures such as germ tubes and appressoria to gain entry into the host while the host uses defense mechanisms to prevent pathogen entry. Penetration was observed at the junctions between neighbouring epidermal cells and occasionally, through the stomata. The pathogen attempted to penetrate and colonize ILL7537, but further fungal advancement appeared to be halted, and A. lentis did not enter the mesophyll. Successful entry and colonization of ILL6002 coincided with structural changes in A. lentis and the onset of necrotic lesions 5–7 days post inoculation. Once inside the leaf, A. lentis continued to grow, colonizing all parts of the leaf followed by plant cell collapse. Pycnidia-bearing spores appeared 14 days post inoculation, which marks the completion of the infection cycle. The use of fluorescent proteins in plant pathogenic fungi together with confocal laser scanning microscopy, provide a valuable tool to study the intracellular dynamics, colonization strategy and infection mechanisms during plant-pathogen interaction.