Protected by a tough outer coat that is impervious to cold, heat, drought and harsh chemicals, anthrax spores can remain dormant in the soil for decades. Once inside a living host, however, they can germinate and begin infecting cells in as little as ten minutes.
Scientists know very little about what triggers an anthrax spore to break dormancy. Identifying the biochemical signals that start the process is an important first step to preventing anthrax infection.
A new study by U-M scientists John A.W. Ireland, health science research fellow, and Philip C. Hanna, assistant professor of microbiology and immunology at the Medical School, shows that germination requires the coordinated activity of several genes, receptor proteins and amino acids in at least two simultaneous signaling pathways. The U-M study, published in the March 2002 issue of the Journal of Bacteriology, is the first to match anthrax genes with specific amino acids and signaling pathways that trigger germination.
Anthrax doesnt rely on a single signal, Hanna says. Endospores have a redundant germination mechanism. Its the bugs way of ensuring that it wont lose its protective armor until conditions are right for germination.
Hanna and Ireland discovered that amino acids, the fundamental building blocks of all proteins in the body, in combination with purine ribonucleosides, the building blocks of DNA and RNA, are triggers for anthrax spore germination. The process appears to begin when receptor proteins on the spores membrane bind to ring-shaped or aromatic structures found on certain amino acids and ribonucleosides.
The receptor protein is the lock, and ring structures are the keys, Ireland says. The only place we know where all the required elements for germination are present is inside our cells, especially our phagocytesthe scavenger cells of the immune system, Ireland explains. But even in the macrophage where conditions are optimum for germination, the spore remains intact until at least two separate signaling pathways are activated.