This is really a story about epigenetics - hereditary information transmitted from parents to offspring via a crust of proteins etc. that cling to, and alter the function of, DNA without changing the DNA itself - but the discovery of a new mechanism is particularly interesting.

When lab-bred female flies are bred with male flies caught in the wild, their progeny are sterile or unable to produce offspring -- a phenomenon called hybrid dysgenesis. But the genetically identical offspring of wild-caught female flies and lab-bred males are fertile. The genetic difference between the lab-bred and wild flies is a single transposon, which is absent in lab strains.

In hybrid dysgenesis, the transmission of the transposon by a parent induces sterility in the offspring unless the offspring also inherits a factor that suppresses the transposon and maintains fertility. Since the phenomenon had only been seen when the transposon-transmitting parent was male, the suppressing factor was thought to be maternally transmitted. But it was never identified.

Hannon's team has now found that the stockpile of maternally derived proteins, RNA, and nourishing raw material in developing fruit fly oocytes, or egg cells, also includes piRNAs. And these maternally deposited piRNAs prove to be essential for mounting a silencing response against transposons.

It's not just DNA that matters, it is also the delivery package. It gets better.

Hannon likens this protection to that afforded by the adaptive immune system which protects against pathogens like bacteria and viruses. "We've evolved ways to transmit immunity from mother to child via the secretion of antibodies," he says, referring to the proteins that can cross the placenta and protect the fetus or get passed on to an infant via breast-milk. "We now have a way in which immunity (against sterility) is passed on from mother to child, in flies but possibly other organisms also, via small RNAs."

In contrast to short-lived adaptive immunity, however, this small RNA-driven immunity has a long reach. The team's experiments show that the effect on fertility doesn't just impact the child alone, but also the next generation. Because the trait – fertility – is controlled or encoded in the RNA, "you're passing on a trait that's essentially not only controlling an event that happens in the organism's adulthood, but is also propagated to the progeny of that organism," explains Hannon. . .

The ability of the mother to transmit epigenetic information can be altered by the environment that she finds herself in. Other researchers have found that raising the temperature in which female flies are reared raises the proportion of fertile progeny.

To the CSHL team, this suggests that "the experience of the mother translates into a dominant effect on the progeny." The group's data suggest that one way that the mother's experience might get communicated to the child is through variations in the populations of small RNAs that get deposited in the oocytes.

Now that one trait has been discovered to be driven by maternally inherited piRNA, Hannon is eager to know if the spectrum of information that's transmitted in this way can be broadened to cover other cellular processes. And of course, it also remains to be seen whether this mechanism of epigenetic inheritance is found in organisms besides fruit flies. "Small RNAs are probably deposited in oocytes of every animal," he hypothesizes.

It's complicated. It's fascinating. All of the bitter disputes of the previous century about adaptive inheritance were conducted without the benefit of good information. I suspect that research of this sort was stigmatized and so retarded a bit for some decades. I suspect that there may be applications in agriculture for insights that come this research. I hope that there are some researchers pursuing this angle.