By KENNETH A. LANDMANThe bacteria that grow at the center of the tropical greenhouse fungus (GANODerma) that causes some of the world’s worst food and fuel problems is a key player in our food system.
That is why researchers have long been searching for ways to cultivate the fungus to produce food, and also to help it survive in the harsh environment of the tropics.
But scientists have been missing out on something crucial in growing the fungus, which is that it produces a toxin that destroys the bacteria’s ability to reproduce.
Now a new study in Nature by the University of Illinois and the University at Buffalo sheds light on how this toxic cocktail works.
In the study, researchers found that in the fungus’s absence, the bacteria that produce the toxin die off.
This is a critical point.
If the bacteria dies off, it is unlikely to produce a toxin to help the fungus survive.
This means the toxin has little effect on the fungus itself, but it is important that the toxin be present for the fungus that produces it to survive.
“When the toxin is present, it really affects how quickly the fungus can reproduce, but also how quickly it dies,” said lead author Rakesh Kumar, a professor of chemical and biomolecular engineering.
The team used a molecular analysis to show that GANODE is a major contributor to the death of the bacterial species that produce and produce the toxins.
The researchers also identified genes that are associated with GANOSEC and are involved in the production of the toxins in the bacteria.
The researchers found the genes are expressed in the guts of the fungus when it produces the toxin.
These genes were also found in the cells of the bacteria in which the toxin was produced.
“The researchers show that the toxins are produced in the gut by the GANO-deficient fungus when the toxin itself is not produced,” said Kumar.
“These toxins are a major factor in the loss of these bacteria.”
In addition to being a key contributor to GANoderm-specific destruction, the toxins also contribute to the loss in the capacity of the G-protein-coupled receptor for growth factor (G-FAT) to promote growth of the gut bacteria.
“It is important to realize that the production and use of the toxin are both dependent on the G protein-couple receptors that regulate G-flux to promote the growth of G-FACTs,” said co-author Kevin Siegel, an assistant professor of chemistry and biological sciences at the University and professor of biological engineering at the UI.
The toxin, however, does not kill the bacteria, it simply disrupts the bacteria by interfering with their ability to produce the toxic proteins.
This may not seem like a big deal, but the toxin does have important implications for human health.
In addition to disrupting the growth and activity of the microbiome, the toxin can be toxic to other organisms.
For example, a previous study showed that it can cause cancer in mice by disrupting the gut microbiota.
In this study, the team found that the enzyme GAP-2, which converts the toxin to GAP, was upregulated in the tumors.
The GAP family of enzymes are a key enzyme that converts the neurotoxic protein ganogen to the toxic protein gandidogen.
The enzymes also have a role in many other functions.
“We are now beginning to understand that the GAP pathway is important for the development of many other enzymes and other proteins in the microbiome,” said Siegel.
“So there is a big picture here.”
To understand how this toxin is produced, the researchers used a synthetic system that synthesizes the toxin in the lab and then used a new method to grow it in the laboratory.
They also sequenced the toxin and its metabolites to find genes that regulate how the toxin functions.
In particular, they found that there are genes that control how the toxins react to the gut flora.
The team used this to show how the GAPP-2 pathway plays a key role in the toxicity of GANode, and it was able to identify several genes that were expressed in both the bacteria and the fungi.
These are genes responsible for how the toxic toxin functions, and the genes were associated with a number of enzymes, including GAP and the enzymes that produce GAP.
The authors also identified several genes related to G-FPACT, which are involved with the production, secretion and elimination of GAP in the stomach and intestines.
“These new studies provide a glimpse into the role of GAPP in the pathogenesis of GANDID and other diseases that affect the gut microbiome,” Kumar said.
“And we have a lot of work ahead of us to understand how the toxicity is produced in this symbiotic relationship.”###This work was supported by grants from the National Institutes of