The influence of human activity on the biosphere is increasing. While direct damage (e.g. habitat destruction) is relatively well understood, many activities affect wildlife in less apparent ways. Here, we investigate how anthropogenic noise impairs foraging, which has direct consequences for animal survival and reproductive success. Noise can disturb foraging via several mechanisms that may operate simultaneously, and thus, their effects could not be disentangled hitherto. We developed a diagnostic framework that can be applied to identify the potential mechanisms of disturbance in any species capable of detecting the noise. We tested this framework using Daubenton's bats, which find prey by echolocation. We found that traffic noise reduced foraging efficiency in most bats. Unexpectedly, this effect was present even if the playback noise did not overlap in frequency with the prey echoes. Neither overlapping noise nor nonoverlapping noise influenced the search effort required for a successful prey capture. Hence, noise did not mask prey echoes or reduce the attention of bats. Instead, noise acted as an aversive stimulus that caused avoidance response, thereby reducing foraging efficiency. We conclude that conservation policies may seriously underestimate numbers of species affected and the multilevel effects on animal fitness, if the mechanisms of disturbance are not considered.

Short-term adjustments of signal characteristics allow animals to maintain reliable communication in noise. Noise-dependent vocal plasticity often involves simultaneous changes in multiple parameters. Here, we quantified for the first time the relative contributions of signal amplitude, duration, and redundancy for improving signal detectability in noise. To this end, we used a combination of behavioural experiments on pale spear-nosed bats (Phyllostomus discolor) and signal detection models. In response to increasing noise levels, all bats raised the amplitude of their echolocation calls by 1.8–7.9 dB (the Lombard effect). Bats also increased signal duration by 13%–85%, corresponding to an increase in detectability of 1.0–5.3 dB. Finally, in some noise conditions, bats increased signal redundancy by producing more call groups. Assuming optimal cognitive integration, this could result in a further detectability improvement by up to 4 dB. Our data show that while the main improvement in signal detectability was due to the Lombard effect, increasing signal duration and redundancy can also contribute markedly to improving signal detectability. Overall, our findings demonstrate that the observed adjustments of signal parameters in noise are matched to how these parameters are processed in the receiver’s sensory system, thereby facilitating signal transmission in fluctuating environments.

Methylation of Lys residues in the tail of the H3 histone is a key regulator of chromatin state and gene expression, conferred by a large family of enzymes containing an evolutionarily conserved SET domain. One of the main types of SET domain proteins are those controlling H3K4 di-and trimethylation. The genome of Arabidopsis (Arabidopsis thaliana) encodes 12 such proteins, including five ARABIDOPSIS TRITHORAX (ATX) proteins and seven ATX-Related proteins. Here, we examined three untilnow-unexplored ATX proteins, ATX3, ATX4, and ATX5. We found that they exhibit similar domain structures and expression patterns and are redundantly required for vegetative and reproductive development. Concurrent disruption of the ATX3, ATX4, and ATX5 genes caused marked reduction in H3K4me2 and H3K4me3 levels genome-wide and resulted in thousands of genes expressed ectopically. Furthermore, atx3/atx4/atx5 triple mutants resulted in exaggerated phenotypes when combined with the atx2 mutant but not with atx1. Together, we conclude that ATX3, ATX4, and ATX5 are redundantly required for H3K4 di-and trimethylation at thousands of sites located across the genome, and genomic features associated with targeted regions are different from the ATXR3/SDG2-controlled sites in Arabidopsis.