Research


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Research project (§ 26 & § 27)
Duration : 2017-09-01 - 2020-08-31

Fungal-plant interactions constitute fine-tuned interplays where each of the participating organisms has evolved efficient strategies to win over the other. To establish a successful infection of a plant host the invading fungal pathogen has to quickly respond and adapt to numerous plant defence mechanisms. This implies a coordinated expression of metabolic and virulence-associated genes, and there is compelling evidence that part of the communication between both interacting organisms is regulated at the level of chromatin. In this project, we strive to unravel chromatin-based mechanisms that govern adequate transcriptomic responses during the host-pathogen interaction using the notorious plant pathogen Fusarium graminearum and wheat (Triticum aestivum) as pathosystem. We have previously identified and characterised a heterochromatin-deficient mutant (Δhep1) that exhibited a hypervirulent phenotype. While most strains deficient for a specific chromatin regulator exhibit a hypo- or avirulent phenotype, deletion of the heterochromatin protein 1-encoding gene (hep1), exhibited a hypervirulence of F. graminearum towards its plant host wheat (J. Strauss and colleagues, unpublished data). This phenotype provides a unique advantage in terms of in planta analyses.
Research project (§ 26 & § 27)
Duration : 2017-08-01 - 2020-07-31

Even though mankind highly depends on plant derived products, our insight into plant specific growth mechanisms is scarce. The plant vacuoles as well as the cell wall are key regulatory factors that jointly control cellular expansion. The process of cell elongation requires both the loosening of cell wall properties and increase in vacuolar volume in a well-orchestrated manner (Löfke et al., eLife 2015; Dünser and Kleine-Vehn, COPB 2015; Scheuring et al., PNAS 2016). However, a growth integrating mechanism, possibly coordinating molecular events in the cell wall and the vacuole, remain currently unknown. Here, we propose that changes in cell wall mechanics integrate vacuolar morphology. We intend to isolate likely cell wall sensors, required to integrate mechanical cues with vacuolar occupancy of the cell. The results of this PhD project might help to elucidate cellular growth control mechanisms contributing to overall plant growth and development.
Research project (§ 26 & § 27)
Duration : 2017-05-20 - 2020-05-19

Alternative splicing allows one gene to produce more than one protein. In many genes, protein information embedded in regions called exons is interrupted by introns, which have to be removed. During alternative splicing, size of some exons changes, or exons can be skipped, therefore an altered protein can be produced. Tight control of alternative splicing has paramount importance as evidenced by linkage of abnormal alternative splicing to numerous human diseases including cancer. Exon skipping is the most frequent alternative splicing event in human; therefore studies of cancer-associated alternative splicing have been well focused on detection and characterization of this type of event. Recently, we have discovered an unusual type of alternative splicing that we named exitron (exonic intron) splicing. Exitrons are internal regions of protein-coding exons and have features of both exons and introns. Strikingly, exitron splicing occurs in many important human protein-coding genes including those involved in cancer. Moreover, we found aberrant exitron splicing events in breast cancer. These findings suggest an overlooked role for exitron splicing in disease. In this proposal, we aim to investigate a link between exitron splicing and cancer so far never explored in different tumours. To this end we will perform computational analyses of multiple data sets derived from various tumours to systematically identify abnormally spliced exitrons. We will confirm computational predictions by experiments with cancer cell lines. Next, using both computational and experimental means we will investigate splicing regulatory elements and splicing factors implicated in aberrant exitron splicing in cancer. Taken together, this project will advance our understanding of the mechanisms of alternative splicing and may lead to the development of novel cancer biomarkers and therapeutic targets.

Supervised Theses and Dissertations