Accurate, high-throughput phenotyping for quantitative traits is a limiting factor for progress in plant breeding. We developed an automated image analysis to measure quantitative resistance to septoria tritici blotch (STB), a globally important wheat disease, enabling identification of small chromosome intervals containing plausible candidate genes for STB resistance. 335 winter wheat cultivars were included in a replicated field experiment that experienced natural epidemic development by a highly diverse but fungicide-resistant pathogen population. More than 5.4 million automatically generated phenotypes were associated with 13,648 SNP markers to perform the GWAS. We identified 26 chromosome intervals explaining 1.9-10.6% of the variance associated with four independent resistance traits. Sixteen of the intervals overlapped with known STB resistance intervals, suggesting that our phenotyping approach can identify simultaneously (i.e., in a single experiment) many previously defined STB resistance intervals. Seventeen of the intervals were less than 5 Mbp in size and encoded only 173 genes, including many genes associated with disease resistance. Five intervals contained four or fewer genes, providing high priority targets for functional validation. Ten chromosome intervals were not previously associated with STB resistance, perhaps representing resistance to pathogen strains that had not been tested in earlier experiments. The SNP markers associated with these chromosome intervals can be used to recombine different forms of quantitative STB resistance that are likely to be more durable than pyramids of major resistance genes. Our experiment illustrates how high-throughput automated phenotyping can accelerate breeding for quantitative disease resistance.

Mobile apps including videos and data collection interfaces could be an interesting alternative in oral cancer research development.

Mammalian male meiosis requires homologous recombination between the X and Y chromosomes. In humans, such recombination occurs exclusively in the short arm pseudoautosomal region (PAR1) of 2.699 Mb in size. Although it is known that complete deletion of PAR1 causes spermatogenic arrest, no studies have addressed to what extent male meiosis tolerates PAR1 size reduction. Here, we report two families in which PAR1 partial deletions were transmitted from fathers to their offspring. Cytogenetic analyses revealed that a ∼400 kb segment at the centromeric end of PAR1, which accounts for only 14.8% of normal PAR1 and 0.26% and 0.68% of the X and Y chromosomes respectively, is sufficient to mediate sex chromosomal recombination during spermatogenesis. These results highlight the extreme recombinogenic activity of human PAR1. Our data, in conjunction with previous findings, indicate that the minimal size requirement of mammalian PARs to maintain male fertility is fairly small.

Oliveira, S.C.; Castroagudin, V.L.; Maciel, J.L.N.; Pereira, D.A.S.; Ceresini, P.C. Cross-resistance to QoI fungicides azoxystrobin and pyraclostrobin in the wheat blast pathogen Pyricularia oryzae in Brazil. Summa Phytopathologica, v.41, n.4, p.298-304, 2015. ABSTRACTand carrier of the non-mutant cyt b gene (haplotype H9), and b) resistant to azoxystrobin and carrier of the G143A mutation in the cyt b gene (H1 haplotype). Fungicides belonging to the same chemical group show cross-resistance. All P. oryzae isolates sensitive to azoxystrobin were also sensitive to pyraclostrobin. Isolates that were resistant to azoxystrobin were also resistant to pyraclostrobin, indicating cross-resistance to both fungicides. Two phenotypic groups were distinguished among the resistant isolates: (A) highly resistant and (B) resistant. P. oryzae isolates with the presence of G143A mutation in the cyt b gene were 42 times more resistant to pyraclostrobin. These high levels of resistance to QoI fungicides may be the result of high selection pressure exerted by consecutive years of strobilurin application for the management of wheat diseases in Brazil.Palavras-chave: estrobilurina, citocromo b, inibidores de quinona oxidase, EC 50 , Triticum aestivum.

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