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Publikationen - Molekulare Signalverarbeitung

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Publikation

Liu, S.; Ziegler, J.; Zeier, J.; Birkenbihl, R. P.; Somssich, I. E.; Botrytis cinerea B05.10 promotes disease development in Arabidopsis by suppressing WRKY33-mediated host immunity Plant Cell Environ. 40, 2189-2206, (2017) DOI: 10.1111/pce.13022

The large WRKY transcription factor family is mainly involved in regulating plant immune responses. Arabidopsis WRKY33 is a key transcriptional regulator of hormonal and metabolic processes towards Botrytis cinerea strain 2100 infection and is essential for resistance. In contrast to B. cinerea strain 2100, the strain B05.10 is virulent on wild‐type (WT) Col‐0 Arabidopsis plants highlighting the genetic diversity within this pathogen species. We analysed how early WRKY33‐dependent responses are affected upon infection with strain B05.10 and found that most of these responses were strongly dampened during this interaction. Ectopic expression of WRKY33 resulted in complete resistance towards this strain indicating that virulence of B05.10, at least partly, depends on suppressing WRKY33 expression/protein accumulation. As a consequence, the expression levels of direct WRKY33 target genes, including those involved in the biosynthesis of camalexin, were also reduced upon infection. Concomitantly, elevated levels of the phytohormone abscisic acid (ABA) were observed. Molecular and genetic studies revealed that ABA negatively influences defence to B05.10 and effects jasmonic acid/ethylene (JA/ET) and salicylic acid (SA) levels. Susceptibility/resistance was determined by the antagonistic effect of ABA on JA, and this crosstalk required suppressing WRKY33 functions at early infection stages. This indicates that B. cinerea B05.10 promotes disease by suppressing WRKY33‐mediated host defences.
Publikation

Delker, C.; Quint, M.; Expression level polymorphisms: heritable traits shaping natural variation Trends Plant Sci. 16, 481-488, (2011) DOI: 10.1016/j.tplants.2011.05.009

Natural accessions of many species harbor a wealth of genetic variation visible in a large array of phenotypes. Although expression level polymorphisms (ELPs) in several genes have been shown to contribute to variation in diverse traits, their general impact on adaptive variation has likely been underestimated. At present, ELPs have predominantly been correlated to quantitative trait loci (eQTLs) that occupy central hubs in signaling networks, which pleiotropically affect numerous traits. To increase the sensitivity of detecting minor effect eQTLs or those that act in a trait-specific manner, we emphasize the need for more systematic approaches. This requires, but is not limited to, refining experimental designs such as reduction of tissue complexity and combinatorial methods including a priori defined networks.
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