(“several species of ticks and mites”)
It’s a dog eat dog world, and bacteria have been living in it for a long time. It’s of no surprise that bacteria have a sophisticated arsenal to compete with each other for valuable resources in the environment. In 2010, work led by University of Washington Department of Microbiology Associate Professor Joseph Mougous uncovered a weaponry system used in this warfare between bacteria. The combatants inject deadly toxins into rival cells.
Now, in a surprising twist, Mougous and colleagues have found that many animals have taken a page from the bacterial playbook. They steal these toxins to fight unwanted microbes growing in or on them. The researchers describe their findings in a report to be published online Nov. 24 in the journal Nature.
“When we started digging into genome databases, we were surprised to find that toxin genes we thought were present only in bacteria were also in several animals,” explained co-author Matt Daugherty, a postdoctoral fellow in the Malik lab. “We immediately started wondering why they were there.”
While such transfer events are common between microbes, very few genes have been reported to jump from bacteria to more complex organisms.
Best guess: There’ll be more.
One problem this creates for Darwinian evolution is this: Determining when a change actually happened in a Darwinian way (natural selection acting on random mutation) as opposed to horizontal gene transfer is now a matter for research, not dogma.
Horizontal gene transfer allows organisms to rapidly acquire adaptive traits1. Although documented instances of horizontal gene transfer from bacteria to eukaryotes remain rare, bacteria represent a rich source of new functions potentially available for co-option2. One benefit that genes of bacterial origin could provide to eukaryotes is the capacity to produce antibacterials, which have evolved in prokaryotes as the result of eons of interbacterial competition. The type VI secretion amidase effector (Tae) proteins are potent bacteriocidal enzymes that degrade the cell wall when delivered into competing bacterial cells by the type VI secretion system3. Here we show that tae genes have been transferred to eukaryotes on at least six occasions, and that the resulting domesticated amidase effector (dae) genes have been preserved for hundreds of millions of years through purifying selection. We show that the dae genes acquired eukaryotic secretion signals, are expressed within recipient organisms, and encode active antibacterial toxins that possess substrate specificity matching extant Tae proteins of the same lineage. Finally, we show that a dae gene in the deer tick Ixodes scapularis limits proliferation of Borrelia burgdorferi, the aetiologic agent of Lyme disease. Our work demonstrates that a family of horizontally acquired toxins honed to mediate interbacterial antagonism confers previously undescribed antibacterial capacity to eukaryotes. We speculate that the selective pressure imposed by competition between bacteria has produced a reservoir of genes encoding diverse antimicrobial functions that are tailored for co-option by eukaryotic innate immune systems. (You have to pay to read the article.)
Follow UD News at Twitter!