The rest is silence.

Over the past several years, RNAi and its related phenomena have emerged not only as a powerful experimental tool but also as a new mode of gene regulation. Through a combination of genetic and biochemical approaches we have learned much about the mechanisms underlying dsRNA responses. However, many of the most intriguing aspects of dsRNA-induced gene silencing have yet to be illuminated. What has become abundantly clear is that the complex and highly conserved biology underlying RNA interference is critical both for genome maintenance and for the development of complex organisms. However, it seems probable that we have only begun to reveal the diversity of biological roles played by RNAi-related processes.     

Why silence is not an option

GM products will continue to be marginalized in Europe as long as industry remains silent.     

The signs of silence

How does auditory cortex respond to silence? In this issue of Neuron, show that activity in macaque auditory cortex is highly structured even in the absence of sensory stimuli. These data reveal a close link between spontaneous neural activity and the functional organization of auditory cortex.     

The silence of the genes

About two years ago, it was recognized that introduction of double-stranded RNA (dsRNA) had a potent effect on gene expression, in particular on mRNA stability. Since then, this process has been found to occur in many different organisms, and to bear a strong resemblance to a previously recognized process in plants, called cosuppression. Both genetic and biochemical studies have started to unravel the mysteries of RNA interference: genes involved in this process are being identified and in vitro studies are giving the first hints of what is happening to both the dsRNA and the affected mRNA molecules after the introduction of the dsRNA.     

Mitochondrial uncoupling protein silence is compromised in photosynthesis and redox poise

Mitochondrial uncoupling proteins play important roles in generation of metabolic thermogenesis, response to stress situations, and regulation of energy metabolism. We demonstrated here that the absence of LeUCP in tomato inhibited photosynthesis using virus-induced gene-silencing approach. A significant decrease in the rate of CO₂ assimilation in LeUCP-silencing plants was observed over a range of different light intensities. Absence of LeUCP resulted in lower net photosynthetic rate, light-saturated rate of the CO₂ assimilation (A _sat), maximum carboxylation rates (V _cmax) and maximum RuBP regeneration rate (J _max). Activities of ribulose-1,5-bisphosphate carboxylase/oxygenase Rubisco and stromal fructose-1,6-bisphosphatase and genes expression levels encoded Calvin cycle enzymes of LeUCP gene-silencing plants were inhibited. However, silencing of LeUCP gene had no effect on F _v/F _m, but decreased photochemical quenching and electron transport rate. Meanwhile, non-photochemical quenching and Je (PSII), the distribution of Je (PCR) and Je (PCO), the content of AsA, NAD, and the ratios of NAD⁺/NADH, AsA/DHA were significantly reduced with increased reactive oxygen species while GSH and GSSG were unaltered. Taken together, these results strongly suggest that LeUCP gene in tomato leaves is crucial in maintaining the redox poise of the mitochondrial electron transport chain to facilitate photosynthetic metabolism.     

Remembering silence.

Polycomb response elements (PREs) are regulatory switch elements that can direct the genes that they control to be either active or silenced. Once decided, this on or off state is maintained through subsequent cell divisions. We do not know how the switching works, or how it is copied to newly replicated chromosomes. Experiments that switch a silenced PRE to an active state have provided insights into both questions. A PRE switched experimentally can remember its previously silenced state and return to it after several cell divisions. In the most recent study of this phenomen on, the data show that several distinct variables affect the ability of PREs to "remember" and restore their previous state. The authors' interpretation of these results is discussed here.     

A new layer of regulation is required to silence the DNA damage checkpoint

Comment on: Wood MD, et al. Cell Cycle 2010; 9:3354-64.