Andreas Peil

Dr. Andreas Peil


Research Focus & Metrics

Academic Career Length

13Years (2014-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

View All Publications
1 August 2020 in Plant Disease
Verified
Journal Article
Open access
APAndrea Patocchi
Andrea Patocchi
AWAndreas Wehrli
Andreas Wehrli
PDPierre-Henri Dubuis
Pierre-Henri Dubuis
AAAnnemarie Auwerkerken
Annemarie Auwerkerken
CLCarmen Leida
Carmen Leida
Vincent BusVincent Bus
Vincent Bus
Apple scab, caused by Venturia inaequalis, is a major fungal disease worldwide. Cultivation of scab-resistant cultivars would reduce the chemical footprint of apple production. However, new apple cultivars carrying durable resistances should be developed to prevent or at least slow the breakdown of resistance against races of V. inaequalis. One way to achieve durable resistance is to pyramid multiple scab resistance genes in a cultivar. The choice of the resistance genes to be combined in the pyramids should take into account the frequency of resistance breakdown and the geographical distribution of apple scab isolates able to cause such breakdowns. In order to acquire this information and to make it available to apple breeders, the VINQUEST project ( www.vinquest.ch ) was initiated in 2009. Ten years after launching this project, 24 partners from 14 countries regularly contribute data. From 2009 to 2018, nearly 9,000 data points have been collected. This information has been used to identify the most promising apple scab resistance genes for developing cultivars with durable resistance, which to date are: Rvi5, Rvi11, Rvi12, Rvi14, and Rvi15. As expected, Rvi1, together with Rvi3 and Rvi8, were often overcome, and have little value for scab resistance breeding. Rvi10 may also belong to this group. On the other hand, Rvi2, Rvi4, Rvi6, Rvi7, Rvi9, and Rvi13 are still useful for breeding, but their use is recommended only in extended pyramids of ≥3 resistance genes.

5 June 2020 in Journal of Plant Pathology
Verified
Journal Article
Closed access
PDF file
APAndreas Peil
Andreas Peil
OEOfere Francis Emeriewen
Ofere Francis Emeriewen
AKAwais Khan
Awais Khan
SKSarah Kostick
Sarah Kostick
MMMickael malnoy
Mickael malnoy

26 April 2019 in Frontiers in Plant Science
Verified
Journal Article
Open access
OEOfere Emeriewen
Ofere Emeriewen
TWThomas Wöhner
Thomas Wöhner
HFHenryk Flachowsky
Henryk Flachowsky
APAndreas Peil
Andreas Peil
The bacterium, Erwinia amylovora, deposits effector proteins such as AvrRpt2EA in to hosts through the type III secretion pathogenicity island to cause fire blight in susceptible Malus genotypes. A single nucleotide polymorphism in the AvrRpt2EA effector plays a key role in pathogen virulence on Malus hosts by exchanging one cysteine to serine in the effector protein sequence. Fire blight resistance quantitative trait loci (QTLs) were detected in a few apple cultivars and wild Malus genotypes with the resistance of wild apples generally found to be stronger than their domestic relatives. The only candidate and functionally analysed fire blight resistance genes proposed are from wild apple genotypes. Nevertheless, the aforementioned AvrRpt2EA SNP and a couple of effector mutants of E. amylovora are responsible for the breakdown of resistance from a few Malus donors including detected QTLs and underlying R-genes. This review summarises a key finding related to the molecular basis underpinning an aspect of virulence of E. amylovora on Malus genotypes, as well as mechanisms of host recognition and specificity, and their implications on the results of genetic mapping and phenotypic studies within the last five to six years. Although the knowledge gained has improved our understanding of the Malus – E. amylovora system, more research is required to fully grasp the resistance mechanisms in this genus especially as they pertain to direct interactions with pathogen effectors.

17 January 2017 in European Journal of Plant Pathology
Verified
Journal Article
Closed access
PDF file
OEOfere Francis Emeriewen
Ofere Francis Emeriewen
APAndreas Peil
Andreas Peil
KRKlaus Richter
Klaus Richter
EZElena Zini
Elena Zini
MHMagda-Viola Hanke
Magda-Viola Hanke
MMMickael malnoy
Mickael malnoy

6 August 2018 in Molecular Breeding
Verified
Journal Article
Open access
PDF file
OEOfere Francis Emeriewen
Ofere Francis Emeriewen
KRKlaus Richter
Klaus Richter
SPStefano Piazza
Stefano Piazza
DMDiego Micheletti
Diego Micheletti
GBGiovanni A. L. Broggini
Giovanni A. L. Broggini
APAndreas Peil
Andreas Peil
Breeding for resistance against the destructive fire blight disease of apples is the most sustainable strategy to control the menace of this disease, and has become increasingly important in European apple breeding programs. Since most cultivars are susceptible, wild accessions have been explored for resistance with quantitative trait loci detected in a few wild species. Fire blight resistance of Malus fusca was described following phenotypic evaluations with a C-type strain of Erwinia amylovora, Ea222_JKI, and the detection of a major QTL on chromosome 10 (Mfu10) of this crabapple. The stability of the resistance of M. fusca and Mfu10 has been evaluated using two other strains, the highly aggressive Canadian S-type strain—Ea3049, and the avrRpt2EA mutant—ZYRKD3-1, both of which overcome the resistance of Malus ×robusta 5, a wild species accession with an already described fire blight resistance gene. To pave the way for positional cloning of the underlying fire blight resistance gene of M. fusca, we have fine mapped the QTL region on linkage group 10 using 1888 individuals and 23 newly developed molecular markers, thus delimiting the interval of interest to 0.33 cM between markers FR39G5T7xT7y/FR24N24RP and FRMf7358424/FR46H22. Tightly linked SSR markers are suitable for marker-assisted selection in breeding programs. Furthermore, a bacterial artificial chromosome (BAC) clone spanning FB_Mfu10 region was isolated and sequenced. One putative fire blight resistance candidate gene of M. fusca was predicted on the sequence of BAC 46H22 within the resistance region that encodes B-lectin and serine/threonine kinase domains.

7 September 2017 in Plant Pathology
Verified
Journal Article
Closed access
PDF file
TWThomas Wöhner
Thomas Wöhner
KRK. Richter
K. Richter
GSG. W. Sundin
G. W. Sundin
YZY. Zhao
Y. Zhao
VSV. O. Stockwell
V. O. Stockwell
APAndreas Peil
Andreas Peil