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Wild Grapes Help Against Climate Change?

What was the topic behind this work? The hot and dry summers cause also in our region to break down grapes in the blossom of their productivity. The cause are wood colonising fungi that are also found in healthy grapes and act there as harmless commensalists. When their host is posed under stress, they suddenly change their behaviour and begin to produce toxins, zu kill their host and extract energy from its corpse to make sex, form fruiting bodies, break out from the wood and spread their spores. ("The rats leave the sinking ship") We wondered, whether we can find grapes that can cope better with this challenge.

How did we approach the question? The key for our research was the Wild Grape Collection established in the Botanical Garden of the KIT. This collection is unique worldwide, because it assembles the entire genetic diversity of the rare European Wild Grapevin (the ancestor of our domesticated Grapevine). In fact, several of these grapes can ward off the attack of wood decaying fungi. Using a connection of molecular, histocheical and Cryo SEM methods we investigated, how their defence works.

What did we get? We could show that fungus and plant run a chemical arm race. The formation of wood and the formation of defence compounds, so called stilbenes, compete for the same entry molecules. The fungus tries to manipulate the grape by chemical signals to make it accumulate as much wood as possible (which is the food for the fungus). The plant, instead, tries to boost the formation of stilbenes. The wild grapes are more powerful in this arm race and channel their metabolism in a way that the potent viniferin trimers are formed that can stop fungal growth. Our knowledge can now help to render grapes, but also city trees, against the consequences of climate change. Our work was published in the high-ranking journal New Phytologist. more...

Press release of the KIT

Cellular Trojans Mitigate Salt Stress

 

What was the topic behind the work? By means of a wooden horse, the Greeks succeeded in entering Troy and conquer the city. Plant cells with their rigid cell wall are quite comparable to the fortress of Troy. To get it under control, usually genetic engineering is employed, introducing DNA into the genome that encodes the desired trait. Is there any other path to manipulate cells immediately, without the detour through the genes? This is what we tried successfully in this work:

How did we approach the question? In cooperation with the team of Ute Schepers (Institute for Toxicology and Genetics) our team succeeded to develop over the years “Chemical Trojans” that can target the mitochondria of plant cells, the organelles, where through respiration energy is generated. Oxygen is actually a risky matter for a cell, because easily reactive oxygen species can result that cause numerous damages. This happens especially, if the stress is exposed to stress and is, by the way, one of the reasons, why we humans often keep bodily damage from stress. Our Trojan Horse did not smuggle in blood-thirsty warriors, but a variant of Coenzyme Q10 that efficiently buffers reactive oxygen species.

What did we achieve? Not only could we demonstrate that pretreatment with this Trojan protects cells against salt stress, but we also cleared up, how this Trojan reaches the heart of the mitochondria. Different from the original concept, this tool does not sneak through the cell membrane, but is taken up with vesicles that pass on their cargo to the endoplasmic reticulum, until the Trojan reaches to the door of the mitochondria. Only here, it permeates the membrane. This is important, because plant cells respond to perturbed integrity of their cell membrane by programmed cell death, a kind of cellular suicide (that, among other purposes, prevents invasions of pathogens). This problem is elegantly circumvented by our "mitochondrial Trojan".

Publication

148. Asfaw KG, Liu Q, Maisch J, Münch S, Wehl I, Bräse S, Bogeski I, Schepers U, Nick P (2019) A Peptoid Delivers CoQ-derivative to Plant Mitochondria via Endocytosis. Nature Sci Rep 9, 9839 - pdf