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The E3 ubiquitin ligase RNF20 regulates chromatin structure by monoubiquitinating histone H2B in transcription. Here, we show that RNF20 is localized to double-stranded DNA breaks (DSBs) independently of H2AX and is required for the DSB-induced H2B ubiquitination. In addition, RNF20 is required for the methylation of H3K4 at DSBs and the recruitment of the chromatin-remodeling factor SNF2h. Depletion of RNF20, depletion of SNF2h, or expression of the H2B mutant lacking the ubiquitination site (K120R) compromises resection of DNA ends and recruitment of RAD51 and BRCA1. Consequently, cells lacking RNF20 or SNF2h and cells expressing H2B K120R exhibit pronounced defects in homologous recombination repair (HRR) and enhanced sensitivity to radiation. Finally, the function of RNF20 in HRR can be partially bypassed by forced chromatin relaxation. Thus, the RNF20-mediated H2B ubiquitination at DSBs plays a critical role in HRR through chromatin remodeling.

Neurons in the lateral intraparietal area, frontal eye field, and superior colliculus exhibit a pattern of activity known as remapping. When a salient visual stimulus is presented shortly before a saccade, the representation of that stimulus is updated, or remapped, at the time of the eye movement. This updating is presumably based on a corollary discharge of the eye movement command. To investigate whether visual areas also exhibit remapping, we recorded from single neurons in extrastriate and striate cortex while monkeys performed a saccade task. Around the time of the saccade, a visual stimulus was flashed either at the location occupied by the neuron's receptive field (RF) before the saccade (old RF) or at the location occupied by it after the saccade (new RF). More than half (52%) of V3A neurons responded to a stimulus flashed in the new RF even though the stimulus had already disappeared before the saccade. These neurons responded to a trace of the flashed stimulus brought into the RF by the saccade. In 16% of V3A neurons, remapped activity began even before saccade onset. Remapping also was observed at earlier stages of the visual hierarchy, including in areas V3 and V2. At these earlier stages, the proportion of neurons that exhibited remapping decreased, and the latency of remapped activity increased relative to saccade onset. Remapping was very rare in striate cortex. These results indicate that extrastriate visual areas are involved in the process of remapping.T he eyes are constantly moving yet we perceive a stable visual world. Psychophysical (1) and neurophysiological (2) experiments indicate that the brain can keep track of the location of visual objects despite eye movements. One neuronal mechanism that may contribute to spatial constancy is updating. Visual neurons in the lateral intraparietal area (LIP), the frontal eye field (FEF), and the intermediate layers of the superior colliculus update, or remap, the representation of a salient stimulus location when the eyes move. In LIP, most neurons (96%) neurons respond when a saccade brings the location of a previously flashed stimulus into the receptive field (RF) (3). Moreover, when the monkey makes a saccade that brings a stationary stimulus into the RF, 44% of LIP neurons, 30% of neurons in intermediate layers of superior colliculus, and 31% of FEF neurons respond at a latency that indicates that remapping is predictive (3-5). This phenomenon may contribute to the brain's ability to maintain a stable, spatially accurate representation despite eye movements. It enables neurons to represent recently stimulated locations immediately at the end of a saccade without the delay associated with retinal reafference. The brain regions in which remapping has been demonstrated to date all are strongly involved in spatial attention and the control of eye movements. We have now asked whether remapping also occurs in extrastriate and striate cortex, which are thought to serve more purely visual functions.We hypothesized that remapping would occur in extrastri...