Although human behavior is much less typecast than that of bees, ants, and termites, our species’ reactions to social situations are also proving to be a matter of differential gene expression. It’s been known for quite a while that social adversity, physical abuse, loneliness, and even grief are associated with increased susceptibility to disease. In “Stress Fractures” you’ll learn about alterations in the expression of immune-system genes that occur as a result of psychological stress, and about the generation of immune cells that can “hide out in the spleen and reemerge months and possibly even years later in response to subsequent stressors, potentially explaining how experiences of social adversity early in life can shape one’s inflammatory landscape as an adult.” Author Daniel Cossins also reports on new evidence that certain stress-induced epigenetic modifications are heritable. The jury is still out on that one, as well as on new research reporting that microRNAs might play a role in passing down stress-influenced phenotypes.
One type of stress that affects all organisms is pathogenic infection. The well-tuned vertebrate immune system employs two strategies to deal with invaders: an immediate and nonspecific innate response, and an adaptive response tailored to the particular pathogen. Prokaryotes facing down an invader were thought to mount nothing more than a fairly simple innate immune response. Eugene Koonin and Mart Krupovic (“A Movable Defense”) recount the pivotal role of mobile genetic elements such as transposons in the establishment of adaptive immunity in bacteria and archaea. A snippet of an invader’s DNA is inserted into a specific region of a host’s genome, the CRISPR cassette, with the help of the Cas1 enzyme; subsequent infection with the same parasite activates the CRISPR-Cas system to produce small RNAs called CRISPR targeting RNAs (crRNAs) that direct the destruction of the invader’s genome. In other words, prokaryotes can remember a particular infection and mount a specific counterattack upon reinvasion. What’s more, this knowledge is passed on to subsequent generations. From extensive comparative genomic studies, Koonin and Krupovic have found that a family of transposons they call casposons lies at the base of the phylogenetic tree in which Cas1 is found: these mobile genetic elements are apparently early ancestors of prokaryote adaptive immunity.
CRISPR-Cas systems—all the rage these days for precision genome editing—are ancient prokaryotic defense mechanisms. But did you know that cheese and yogurt manufacturers rely on the immune systems of bacterial starter cultures to attack viruses that can ruin dairy products? Associate Editor Kerry Grens describes the vaccination of bacterial strains to ramp up their CRISPR-Cas systems, making them better pathogen destroyers and saving businesses a ton of money in the process.
Further insights into the mechanisms of group living and defense against outsiders lie in wait, whether they’re buried deep in the genomes of people suffering social stress, in the epigenetic programs of eusocial ant species, or at the bottom of your yogurt cup. This issue celebrates the scientists who are unlocking the secrets of our very social world.
Mary Beth Aberlin Editor-in-Chief email@example.com