Image from Zina Deretsky, National Science Foundation.
Showing that there are more similarities between humans and plants than many of us would care to think, scientists from the Virginia Bioinformatics Institute (VBI) have just announced that they have discovered a mechanism that enables fungi to infect plants and cause disease. They suggest that the same mechanism allows some fungi to infect the cells of people.
The explanation of how these fungi operate is complex and the following simplification undoubtedly omits important details, but hopefully it conveys the gist of the research. Those readers eager for the full details can follow through on the references below.
It appears that fungi, and some microbes that look like fungi (oomycetes), are able to produce effector molecules which are a little like commandos, or the SAS. These effector molecules (a type of protein) attack the walls of cells, penetrate inside and then disable the defence mechanisms of the cell, leaving it open to invading fungi or oomycetes. These then bring disease into the cell. The Irish Potato Famine was one result of such a disease attack and other such diseases include Sudden Oak Death and Rhododendron Root Rot.
This much was already known. And bacteria were known to be able to use a needle-like protuberance to puncture a cell's walls and to inject their effector molecules into the cell, but the mechanism used by fungi and oomycetes had previously been undiscovered. The latest research is the identification of that mechanism. It seems that they must first bind onto a specific lipid molecule on the cell surface. The lipid is phosphatidylinositol 3-phosphate (PtdIns3P or PI3P) and Professor Brett Tyler of VBI explains, "The nasty proteins enter by hitching a ride on a lipid raft, a region of the cell's outer membrane that can be internalized by the cell. The lipid acts as a bridge between the effector protein and the raft, and in doing so helps to unlock the door for entry of the disease-causing proteins into the cell."
Apparently some fungi/oomycetes use the same mechanism for breaking into human cells.
Having identified the modus operandi for the break-in, scientists are now able to design methods to prevent it occurring. Shiv Kale, a graduate student at VBI and one of the lead authors on the study, remarked: "We were able to block the entry process of the disease-related proteins using two types of inhibitors. The first group of inhibitors covers the lipid so that the pathogen cannot get access to it. The second jams the site on the protein that normally binds the lipid."
Virginia Tech - home of VBI
Surprising aspects of this research include
- The novelty and simplicity of the mechanism used by fungi and oomycetes to insert their effectors into host cells.
- The discovery that fungi and oomycetes use the same binding mechanism to introduce effectors into plant cells, even though these two classes of microbes are evolutionarily distinct from one another.
- The presence of an abundance of the binding lipids on the surfaces of plant cells, animal cells, and some human cells. This discovery suggests that fungal and oomycete effectors might also enter animal and human cells through the same newly-discovered method they use to enter plants. It also suggests that this phenomenon may, in fact, be an attack mechanism common to fungal and oomycete diseases of plants, animals and humans.
The research is published in the journal, Cell
Sources: https://www.vbi.vt.edu/public_relations/press_releases/scientists_discover_how_deadly_fungal_microbes_enter_host_cells , http://www.eurekalert.org/pubnews.php and http://www.sciencedaily.com/releases/2010/07/100722132338.htm