piRNA involvement in genome stability and human cancer.

PIWI-interacting RNAs (piRNAs) are a large family of small, single-stranded, non-coding RNAs present throughout the animal kingdom. They form complexes with several members of the PIWI clade of Argonaute proteins and carry out regulatory functions. Their best established biological role is the inhibition of transposon mobilization, which they enforce both at the transcriptional level, through regulation of heterochromatin formation, and by promoting transcript degradation. In this capacity, piRNAs and PIWI proteins are at the heart of the germline cells' efforts to preserve genome integrity. Additional regulatory roles of piRNAs and PIWI proteins in gene expression are becoming increasingly apparent.PIWI proteins and piRNAs are often detected in human cancers deriving from germline cells as well as somatic tissues. Their detection in cancer correlates with poorer clinical outcomes, suggesting that they play a functional role in the biology of cancer. Nonetheless, the currently available information, while highly suggestive, is still not sufficient to entirely discriminate between a 'passenger' role for the ectopic expression of piRNAs and PIWI proteins in cancer from a 'driver' role in the pathogenesis of these diseases. In this article, we review some of the key available evidence for the role of piRNAs and PIWI in human cancer and discuss ways in which our understanding of their functions may be improved.

The effects of nicotine on cone and rod b-wave responses in larval zebrafish.

Acetylcholine is present in and released from starburst amacrine cells in the inner plexiform layer (IPL), but its role in retinal function except, perhaps, in early development, is unclear. Nicotinic acetylcholine receptors are thought to be present on ganglion, amacrine, and bipolar cell processes in the IPL, and it is known that acetylcholine increases the spontaneous and light-evoked responses of retinal ganglion cells. The effects of acetylcholine on bipolar cells are not known, and here we report the effects of nicotine on the b-wave of the electroretinogram in larval zebrafish. The b-wave originates mainly from ON-bipolar cells, and the larval zebrafish retina is cone-dominated. Only small rod responses can be elicited with dim lights in wild-type larval zebrafish retinas, but rod responses can be recorded over a range of intensities in a mutant ( n o optokinetic response f ) fi sh that has no cone function. We fi nd that nicotine strongly enhances cone-driven b-wave response amplitudes but depresses rod driven b-wave response amplitudes without, however, affecting rod- or cone-driven b-wave light sensitivity.