During Arabidopsis embryo development, cotyledon primordia are generated at transition stage from precursor cells that are not derived from the embryonic shoot apical meristem (SAM). To date, it is not known which genes specifically instruct these precursor cells to elaborate cotyledons, nor is the role of auxin in cotyledon development clear. In laternemutants, the cotyledons are precisely deleted, yet the hypocotyl and root are unaffected. The laterne phenotype is caused by a combination of two mutations: one in the PINOID (PID) gene and another mutation in a novel locus designated ENHANCER OF PINOID (ENP). The expression domains of shoot apex organising genes such as SHOOT MERISTEMLESS (STM) extend along the entire apical region of laterne embryos. However, analysis of pid enp stm triple mutants shows that ectopic activity of STM does not appear to cause cotyledon obliteration. This is exclusively caused by enp in concert with pid. In pinoid embryos, reversal of polarity of the PIN1 auxin transport facilitator in the apex is only occasional, explaining irregular auxin maxima in the cotyledon tips. By contrast, polarity of PIN1:GFP is completely reversed to basal position in the epidermal layer of the laterne embryo. Consequently auxin, which is believed to be essential for organ formation, fails to accumulate in the apex. This strongly suggests that ENP specifically regulates cotyledon development through control of PIN1 polarity in concert with PID.
Fusarium head blight (FHB), mainly caused by Fusarium graminearum and F. culmorum, can significantly reduce the grain quality of wheat (Triticum aestivum L.) due to mycotoxin contamination. The objective of this study was to identify quantitative trait loci (QTLs) for FHB resistance in a winter wheat population developed by crossing the resistant German cultivar Dream with the susceptible British cultivar Lynx. A total of 145 recombinant inbred lines (RILs) were evaluated following spray inoculation with a F. culmorum suspension in field trials in 2002 in four environments across Germany. Based on amplified fragment length polymorphism and simple sequence repeat marker data, a 1,734 cM linkage map was established assuming that the majority of the polymorphic parts of the genome were covered. The area under disease progress curve (AUDPC) was calculated based on the visually scored FHB symptoms. The population segregated quantitatively for FHB severity. Composite interval mapping analysis for means across the environments identified four FHB resistance QTLs on chromosomes 6AL, 1B, 2BL and 7BS. Individually the QTLs explained 19%, 12%, 11% and 21% of the phenotypic variance, respectively, and together accounted for 41%. The QTL alleles conferring resistance on 6AL, 2BL and 7BS originated from cv. Dream. The resistance QTL on chromosome 6AL partly overlapped with a QTL for plant height. The FHB resistance QTL on 7BS coincided with a QTL for heading date, but the additive effect on heading date was of minor importance. The resistance QTL on chromosome 1B was associated with the T1BL.1RS wheat-rye translocation of Lynx.
Fusarium head blight (FHB) resistance is of particular importance in wheat breeding programmes due to the detrimental effects of this fungal disease on human and animal health, yield and grain quality. Segregation for FHB resistance in three European winter wheat populations enabled the identification of resistance loci in well-adapted germplasm. Populations obtained from crosses of resistant cultivars Apache, History and Romanus with susceptible semi-dwarfs Biscay, Rubens and Pirat, respectively, were mapped and analysed to identify quantitative trait loci (QTL) for FHB severity, ear emergence time and plant height. The results of the present study together with previous studies in UK winter wheat indicated that the semi-dwarfing allele Rht-D1b seems to be the major source for FHB susceptibility in European winter wheat. The high resistance level of the cultivars Romanus and History was conditioned by several minor resistance QTL interacting with the environment and the absence of Rht-D1b. In contrast, the semi-dwarf parents contributed resistance alleles of major effects apparently compensating the negative effects of Rht-D1b on FHB reaction. The moderately resistant cultivar Apache contributed a major QTL on chromosome 6A in a genome region previously shown to carry resistance loci to FHB. A total of 18 genomic regions were repeatedly associated with FHB resistance. The results indicate that common resistance-associated genes or genomic regions are present in European winter wheats.
The inheritance of extreme resistance to PVY (Ry (sto)) by a single dominant locus was confirmed by obtaining a 1:1 segregation ratio in a virus inoculation test with 28 resistant (Ryry) to 29 susceptible (ryry) anther culture-derived dihaploid lines (2n=2x=24) from cv. "Assia" (2n=4x=48) having extreme resistance derived from Solanum stoloniferum in simplex constitution (Ryryryry). Twelve Ry (sto) markers selected in AFLP assays using bulked segregant analysis were applied to 106 tested potato cultivars from Germany, The Netherlands and Poland and 19 potato cultivars were identified by these markers as extremely resistant to PVY in alignment with phenotypic data. The locus for extreme resistance (Ry (sto)) to PVY was mapped on chromosome XII co-segregating with the SSR marker STM 0003. The utility of anther-culture derived dihaploid potatoes for genetic marker development was demonstrated. Marker transferability from diploids to tetraploids provides an optimistic potential for marker-assisted selection in potato breeding programs.
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