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We present oyster larval microbiota from two feeding studies, in which wild type and low-salinity tolerant lines were either fed or starved. In one study, all larvae unexpectedly died, which was concurrent with an event in which all larvae in an adjoining oyster hatchery also died. In the other study, no crash occurred in either the study or hatchery. In both cases, larvae were collected and stored frozen, and microbial and host DNA was isolated by phenol-chloroform extraction. Both host 18 s rRNA genes and microbial 16 and 18 s rRNA genes were sequenced using universal primers. We present raw sequences, the pipeline that was used to quantify amplicon sequence variants, and our analysis pipeline that we used to describe how the overall microbial community varied between projects (crashed and non-crashed), feeding status (fed vs not), and strain (wild vs not). These data will be valuable to anyone interested in the microbiota of larval oysters, especially anyone interested in exploring hatchery crashes, effects of starvation, or strain level differences. They also contain a reproducible pipeline of amplicon analysis of host associated microbiota which may serve as a template for other studies. These data are a co-submission to a manuscript submitted to Aquaculture by Matthew grey et al. (2021) entitled Hatchery crashes among shellfish research hatcheries along the Atlantic coast of the United States: a case study at Horn Point Laboratory oyster hatchery. (Manuscript#: AQUACULTURE-D-21–01351R1)

Ocean acidification (OA) is altering the chemistry of the world's oceans at rates unparalleled in the past roughly 1 million years. Understanding the impacts of this rapid change in baseline carbonate chemistry on marine organisms needs a precise, mechanistic understanding of physiological responses to carbonate chemistry. Recent experimental work has shown shell development and growth in some bivalve larvae, have direct sensitivities to calcium carbonate saturation state that is not modulated through organismal acid-base chemistry. To understand different modes of action of OA on bivalve larvae, we experimentally tested how pH, PCO2, and saturation state independently affect shell growth and development, respiration rate, and initiation of feeding in Mytilus californianus embryos and larvae. We found, as documented in other bivalve larvae, that shell development and growth were affected by aragonite saturation state, and not by pH or PCO2. Respiration rate was elevated under very low pH (~7.4) with no change between pH of ~ 8.3 to ~7.8. Initiation of feeding appeared to be most sensitive to PCO2, and possibly minor response to pH under elevated PCO2. Although different components of physiology responded to different carbonate system variables, the inability to normally develop a shell due to lower saturation state precludes pH or PCO2 effects later in the life history. However, saturation state effects during early shell development will carry-over to later stages, where pH or PCO2 effects can compound OA effects on bivalve larvae. Our findings suggest OA may be a multi-stressor unto itself. Shell development and growth of the native mussel, M. californianus, was indistinguishable from the Mediterranean mussel, Mytilus galloprovincialis, collected from the southern U.S. Pacific coast, an area not subjected to seasonal upwelling. The concordance in responses suggests a fundamental OA bottleneck during development of the first shell material affected only by saturation state.