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Feussner, I.

Publications and source records attributed to Feussner, I..

39 records · Page 3Linked to original sources

Arabidopsis mlo3 mutant plants exhibit spontaneous callose deposition and signs of early leaf senescence

The family of Mildew resistance Locus O (MLO) proteins is best known for its profound effect on the outcome of powdery mildew infections: when the appropriate MLO protein is absent, the plant is fully resistant to otherwise virulent powdery mildew fungi. However, most members of the MLO protein family remain functionally unexplored. Here, we investigate Arabidopsis thaliana MLO3, the closest relative of AtMLO2, AtMLO6 and AtMLO12, which are the Arabidopsis MLO genes implicated in the powdery mildew interaction. The co-expression network of AtMLO3 suggests association of the gene with plant defense-related processes such as salicylic acid homeostasis. Our extensive analysis shows that mlo3 mutants are unaffected regarding their infection phenotype upon challenge with the powdery mildew fungi Golovinomyces orontii and Erysiphe pisi, the oomycete Hyaloperonospora arabidopsidis, and the bacterial pathogen Pseudomonas syringae (the latter both in terms of basal and systemic acquired resistance), indicating that the protein does not play a major role in the response to any of these pathogens. However, mlo3 genotypes display spontaneous callose deposition as well as signs of early senescence in six-or seven-week-old rosette leaves in the absence of any pathogen challenge, a phenotype that is reminiscent of mlo2 mutant plants. We hypothesize that de-regulated callose deposition in mlo3 genotypes is the result of a subtle transient aberration of salicylic acid-jasmonic acid homeostasis during development.

plant biology↗

Pheophorbide a, a chlorophyll catabolite may regulate jasmonate signalling during dark-induced senescence in Arabidopsis

Chlorophyll degradation is one of the most visible landmarks of leaf senescence. During senescence, chlorophyll is degraded in the multi-step pheophorbide a oxygenase (PAO)/phyllobilin pathway, which is tightly regulated at the transcriptional level. This regulation allows a coordinated and efficient remobilisation of nitrogen towards sink organs. Taking advantage of combined transcriptome and metabolite analyses during dark-induced senescence of Arabidopsis thaliana mutants deficient in key steps of the PAO/phyllobilin pathway, we show an unanticipated role for one of the pathway intermediates, i.e. pheophorbide a. Both jasmonic acid-related gene expression and jasmonic acid precursors specifically accumulated in pao1, deficient in PAO. We propose that pheophorbide a, the last intact porphyrin intermediate of chlorophyll degradation and unique pathway bottleneck, has been recruited as a signalling molecule of the chloroplast metabolic status. Our work challenges the assumption that chlorophyll breakdown is merely a senescence output, but propose that the flux of pheophorbide a through the pathway acts in a feed-forward loop that remodels the nuclear transcriptome and controls the pace of chlorophyll degradation in senescing leaves.\n\nSummaryTranscriptome and metabolite profiles of key chlorophyll breakdown mutants reveal complex interplay between speed of chlorophyll degradation and jasmonic acid signalling\n\nFinancial sourcesThis work was supported by the European Union (Plant Fellow program), the Swiss National Foundation/ERA-NET (grant N{degrees} 163504) and the German Research Foundation (DFG, grant N{degrees} INST 186/822-1).

plant biology↗

Cyanophage-encoded lipid-desaturases: oceanic distribution, diversity and function

Cyanobacteria are among the most abundant photosynthetic organisms in the oceans; viruses infecting cyanobacteria (cyanophages) can alter cyanobacterial populations, and therefore affect the local food web and global biochemical cycles. These phages carry auxiliary metabolic genes (AMGs), which rewire various metabolic pathways in the infected host cell, resulting in increased phage fitness. Coping with stress resulting from photodamage appears to be a central necessity of cyanophages, yet the overall mechanism is poorly understood. Here we report a novel, widespread cyanophage AMG, encoding a fatty acid desaturase (FAD), found in two genotypes with distinct geographical distribution. FADs are capable of modulating the fluidity of the hosts membrane, a fundamental stress response in living cells. We show that both viral fatty acid desaturases (vFADs) families are {Delta}9 lipid desaturases, catalyzing the desaturation at carbon 9 in C16 fatty acid chains. In addition, we present the first fatty acid profiling for marine cyanobacteria, which suggests a unique desaturation pathway of medium to long chain fatty acids no longer than C16, in accordance to the vFADs activity. Our findings suggest that cyanophages fiddle with the infected hosts cell, leading to increased photoprotection and potentially enhancing viral-encoded photosynthetic proteins, resulting in a new viral metabolic network.

microbiology↗