Using a limited mapping strategy to identify major QTLs for resistance to grapevine powdery mildew (Erysiphe necator) and their use in marker-assisted breeding

A limited genetic mapping strategy based on simple sequence repeat (SSR) marker data was used with five grape populations segregating for powdery mildew (Erysiphe necator) resistance in an effort to develop genetic markers from multiple sources and enable the pyramiding of resistance loci. Three populations derived their resistance from Muscadinia rotundifolia ‘Magnolia’. The first population (06708) had 97 progeny and was screened with 137 SSR markers from seven chromosomes (4, 7, 9, 12, 13, 15, and 18) that have been reported to be associated with powdery or downy mildew resistance. A genetic map was constructed using the pseudo-testcross strategy and QTL analysis was carried out. Only markers from chromosome 13 and 18 were mapped in the second (04327) and third (06712) populations, which had 47 and 80 progeny, respectively. Significant QTLs for powdery mildew resistance with overlapping genomic regions were identified for different tissue types (leaf, stem, rachis, and berry) on chromosome 18, which distinguishes the resistance in ‘Magnolia’ from that present in other accessions of M. rotundifolia and controlled by the Run1 gene on chromosome 12. The ‘Magnolia’ resistance locus was termed as Run2.1. Powdery mildew resistance was also mapped in a fourth population (08391), which had 255 progeny and resistance from M. rotundifolia ‘Trayshed’. A locus accounting for 50% of the phenotypic variation mapped to chromosome 18 and was named Run2.2. This locus overlapped the region found in the ‘Magnolia’-based populations, but the allele sizes of the flanking markers were different. ‘Trayshed’ and ‘Magnolia’ shared at least one allele for 68% of the tested markers, but alleles of the other 32% of the markers were not shared indicating that the two M. rotundifolia selections were very different. The last population, 08306 with 42 progeny, derived its resistance from a selection Vitis romanetii C166-043. Genetic mapping discovered a major powdery mildew resistance locus termed Ren4 on chromosome 18, which explained 70% of the phenotypic variation in the same region of chromosome 18 found in the two M. rotundifolia resistant accessions. The mapping results indicate that powdery mildew resistance genes from different backgrounds reside on chromosome 18, and that genetic markers can be used as a powerful tool to pyramid these loci and other powdery mildew resistance loci into a single line

The effects of applied water at various fractions of measured evapotranspiration on water relations and vegetative growth of Thompson Seedless grapevines

Vegetative growth and water relations of Thompson Seedless grapevines in response to applied water amounts at various fractions of measured grapevine ETc were quantified. Treatments ranged from no applied water up to 1.4 times the water used by vines growing in a weighing lysimeter. All treatments were irrigated at the same frequency as the vines in the lysimeter (whenever they used 2 mm of water), albeit at their respective fraction. Soil water content and midday leaf water potential (Ψl) were measured routinely in four of the irrigation treatments across years. The amount of water depleted in the soil profile ranged from 190 mm for the 0.2 treatment in 1993 to no water depletion for the 1.4 treatment in 1992. The irrigation treatments significantly affected midday Ψl, total shoot length, leaf area per vine, pruning weights and trunk diameter; as applied water decreased so did vegetative growth. Pruning weights were a linear function of the seasonal, mean midday Ψl across growing seasons. The application of water amounts in excess of evapotranspiration negatively affected vegetative growth some of the years. A companion paper will demonstrate that over-irrigation can negatively affect reproductive growth of this grape cultivar due to excess vegetative growth

Gerontobiology of the Hair Follicle

NoThe word ¿gerontology¿ is familiar to most of us as a term that captures the study of the social, psychological, and biological aspects of aging. However, its derivative ¿gerontobiology¿ as applied to the hair follicle is more concerned with the latter aspect ¿ the biology of aging in the hair follicle mini-organ. As with any complex multicellular tissue system, the hair follicle is prone to broadly similar underlying processes that determine the functional longevity of organs and tissues. No matter how complex the tissue system is, it will contain cells that eventually lose functionality, reproductive potential and will ultimately die. The hair follicle is somewhat unusual among mammalian tissues in that it is a veritable histologic mélange of multiple cell types (e.g., epithelial, mesenchymal and neuro-ectodermal) that function contemporaneously in all stages of their life histories e.g., stem cells, transit-amplifying cells, and terminally differentiating cells. Some of these interactive cell systems appear to be nonessential for overall hair follicle survival (e.g., melanocytes). However, strikingly graying hair follicles may grow even more vigorously than their pigmented predecessors. Moreover, the hair follicle is unique in the adult mammal in that it follows a tightly regulated script of multiple lifelong cycles of cellular birth, proliferation, differentiation, and death. Powerful evolutionary selection ensures that the hair follicle is, in the main, hardwired against significant aging-related loss of function, even after 12 or more decades of life ¿ although some would argue with this view, if only on purely cosmetic grounds. Processes underlying aging in general, e.g., oxidative damage, telomere shortening, age-relating deficiencies related to nuclear/mitochondrial DNA damage and repair as well as age-related reductions in the cells¿ energy supply, will all impact on whether some follicular cell subpopulations will enter cellular senescence. This chapter will focus on how gerontobiology of the hair follicle may impact on certain aspects of hair fiber phenotype