A high rate of mutations also disturbs gametogenesis the process of creating viable sex cells and can result in sterility. Piwi proteins and piRNAs form something akin to an immune system in sex cells that guards against transposon-inflicted genome damage.
Solving the fruit fly fertility puzzle
The CSHL team wondered whether piRNAs were also the key to a long-standing conundrum about fertility in fruit flies. 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.
Inheritance via small RNAs
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 antibodie
|Contact: Hema Bashyam|
Cold Spring Harbor Laboratory