The acoustic environment before and during the SARS-CoV-2 lockdown in a major German city as measured by ecoacoustic indices.

The SARS-CoV-2 pandemic drastically changed daily life. Lockdown measures resulted in reduced traffic mobility and, subsequently, a changed acoustic environment. The exceptional lockdown was used to analyze its impact on the urban acoustic environment using ecoacoustic indices. Using data from 22 automated sound recording devices located in 9 land use categories (LUCs) in Bochum, Germany, the normalized difference soundscape index (NDSI) and Bioacoustics index (BIO) were explored. The NDSI quantifies the proportion of anthropophonic to biophonic sounds, and BIO quantifies the total sound activities of biological sources. The mean differences and standard deviation (SD) were calculated 5 weeks before and 5 weeks during the first lockdown. Pronounced peaks for the NDSI and BIO before lockdown that diminished markedly during lockdown were observed, however, with distinct differences in terms of the LUC. The mean NDSI increased from 0.00 (SD = 0.43) to 0.15 (SD = 0.50), the mean BIO decreased from 4.74 (SD = 2.64) to 4.03 (SD = 2.66). Using the NDSI and BIO together reveals that changes of the acoustic environment during lockdown are mainly driven by decreased anthropophonic sound sources. These results suggest that further studies are needed to tailor ecoacoustic indices more accurately to conditions of the urban environment.

The NosX and NirX proteins of Paracoccus denitrificans are functional homologues: their role in maturation of nitrous oxide reductase.

The nos (nitrous oxide reductase) operon of Paracoccus denitrificans contains a nosX gene homologous to those found in the nos operons of other denitrifiers. NosX is also homologous to NirX, which is so far unique to P. denitrificans. Single mutations of these genes did not result in any apparent phenotype, but a double nosX nirX mutant was unable to reduce nitrous oxide. Promoter-lacZ assays and immunoblotting against nitrous oxide reductase showed that the defect was not due to failure of expression of nosZ, the structural gene for nitrous oxide reductase. Electron paramagnetic resonance spectroscopy showed that nitrous oxide reductase in cells of the double mutant lacked the Cu(A) center. A twin-arginine motif in both NosX and NirX suggests that the NosX proteins are exported to the periplasm via the TAT translocon.