Plant apoplast contains various antimicrobial peptides e.g., defensins. As part of their antifungal mode of action, these defensins (not all defensins) are known to interact specifically with membrane-resident bioactive phospholipids, such as PA, PI(4,5)P2 with high affinity. We know that these pathogens have different life style. Very importantly, when biotrophic pathogens thrive in the apoplst, they encounter various antifungal proteins and fungus needs to protect itself from these proteins which subsequently determine the outcome. However, necrotrophic pathogens produce different cell wall-degrading enzymes (CWDEs) and toxins to kill the host plant cell. When necrotrophic pathogens damage the cell wall and plasma membrane, the antimicrobial peptides (e.g., defensins) which are present in the apoplast, may encounter plant membrane-resident bioactive phospholipids. Do you think these defensins highly interact with plant phospholipids (instead of fungal membrane-resident bioactive phospholipids) and indirectly regulate its own plant lipid metabolism? If so, why does it prefer binding to its own phospholipids? Does this non-specific interaction leads to toxicity to the plant cells? What about binding to fungal membrane-resident bioactive phospholipids? Does defensin loses it ability to bind to fungal phospholipids, subsequently paving the way to infect the plant? How do transgenic (and also non-transgenic) plants over expressing phospholipid-binding proteins (e.g., defensins) control itself of these non-specific interactions? Do you think the change in the environment (e.g., pH) can limit these non-specific interactions in both non-transgenic and overexpressing plants ?
Cellulose is not digested in human beings because of the absence of cellulases. If peptides are not bound to its phospholipids, might be because of lack of receptors, might peptides are secreted in special vesicles, or might these peptides are formed in inactive form.
Dear Siva, You have a lot of very interesting questions there and I don't think they can be answered just yet without resorting to conjecture. what is known at present is that there are general reasons as to why fungal membranes are more sensitive to defensins and this will include the presence of differing sterols and the presentation of charged surfaces as well as the distribution of various lipids frim one leaflet to another. For those defensins that do have a specific interactions with e.g. PI lipids then the accessibility of these lipids will be important. You may also consider that the mechanism of action of plant defensins has no been investigated in much detail and that they may have other roles beyond a simple fungicidal activity (i.e. signalling). I think you have devised an interesting research programme with your questions and could spend many fruitful years providing a much more detailed understanding than what is currently available.
- Badges
- Science topic
- Similar topics
- Biological Science
- Biota
- Eukaryota
- Fungi