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Turbulence and sound are important cues for oyster reef larval recruitment. Numerous studies have found a relationship between turbulence intensity and swimming behaviors of marine larvae, while others have documented the importance of sounds in enhancing larval recruitment to oyster reefs. However, the relationship between turbulence and the reef soundscape is not well understood. In this study we made side-by-side acoustic Doppler velocimeter turbulence measurements and hydrophone soundscape recordings over 2 intertidal oyster reefs (1 natural and 1 restored) and 1 adjacent bare mudflat as a reference. Sound pressure levels (SPL) were similar across all three sites, although SPL >  2000 Hz was highest at the restored reef, likely due to its larger area that contained a greater number of sound-producing organisms. Flow noise (FN), defined as the mean of pressure fluctuations recorded by the hydrophone atf<  100 Hz, was significantly related to mean flow speed, turbulent kinetic energy, and turbulence dissipation rate (ε), agreeing with theoretical calculations for turbulence. Our results also show a similar relationship between ε andFNto what has been previously reported for ε vs. downward larval swimming velocity (w_b), with bothFNandw_bdemonstrating rapid growth at ε >  0.1 cm²s⁻³. These results suggest that reef turbulence and sounds may attract oyster larvae in complementary and synergistic ways. 

Abstract Cyclic guanosine monophosphate-adenosine monophosphate (cGAMP), produced by cyclic GMP-AMP synthase (cGAS), stimulates the production of type I interferons (IFN). Here we show that cGAMP activates DNA damage response (DDR) signaling independently of its canonical IFN pathways. Loss of cGAS dampens DDR signaling induced by genotoxic insults. Mechanistically, cGAS activates DDR in a STING-TBK1-dependent manner, wherein TBK1 stimulates the autophosphorylation of the DDR kinase ATM, with the consequent activation of the CHK2-p53-p21 signal transduction pathway and the induction of G1 cell cycle arrest. Despite its stimulatory activity on ATM, cGAMP suppresses homology-directed repair (HDR) through the inhibition of polyADP-ribosylation (PARylation), in which cGAMP reduces cellular levels of NAD + ; meanwhile, restoring NAD + levels abrogates cGAMP-mediated suppression of PARylation and HDR. Finally, we show that cGAMP also activates DDR signaling in invertebrate species lacking IFN ( Crassostrea virginica and Nematostella vectensis ), suggesting that the genome surveillance mechanism of cGAS predates metazoan interferon-based immunity.