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1. Temperature-dependent effects on fecundity in a serial broadcast spawning fish after whole-life high CO2 exposure

   https://doi.org/10.1093/icesjms/fsab217  

   Concannon, Callie A; Cross, Emma L; Jones, Lucas F; Murray, Christopher S; Matassa, Catherine M; McBride, Richard S; Baumann, Hannes (November 2021, ICES Journal of Marine Science)

   Browman, Howard (Ed.)

   Abstract Experiments examining fish sensitivities to future oceanic CO2 levels have greatly expanded over past decades and identified many potentially affected traits. Curiously, data on reproductive trait responses to high CO2 are still scarce, despite their strong link to Darwinian fitness and thus to population vulnerability to ocean acidification. We conducted two rearing experiments on the first broadcast-spawning marine fish model (Atlantic silverside, Menidia menidia) to examine how long-term and novel whole life-cycle exposures to predicted future CO2 levels (∼2,000 µatm) affect laboratory spawning, temperature-specific reproductive investment, fecundity, and size distributions of maturing oocytes. At low temperatures (17°C), female body size and therefore potential fecundity (FPot, oocytes/female) slightly increased with CO2, while relative fecundity (FRel, oocytes/g female) remained unaffected. At high temperatures (24°C), high CO2 substantially reduced both FPot (−19%) and FRel (−28%) relative to control treatments. Irrespective of CO2, females at 24°C grew larger and heavier than those at 17°C, and although larger females produced larger oocytes at some developmental stages, they also had lower gonadosomatic indices and lower FRel. Our findings contrast with most previous studies and thus highlight the need to investigate reproductive impacts of increasing CO2 on multiple fish species with contrasting life history strategies. 

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2. You Better Repeat It: Complex CO2 × Temperature Effects in Atlantic Silverside Offspring Revealed by Serial Experimentation

   https://doi.org/10.3390/d10030069  

   Murray, Christopher; Baumann, Hannes (September 2018, Diversity)

   null (Ed.)

   Concurrent ocean warming and acidification demand experimental approaches that assess biological sensitivities to combined effects of these potential stressors. Here, we summarize five CO2 × temperature experiments on wild Atlantic silverside, Menidia menidia, offspring that were reared under factorial combinations of CO2 (nominal: 400, 2200, 4000, and 6000 µatm) and temperature (17, 20, 24, and 28 °C) to quantify the temperature-dependence of CO2 effects in early life growth and survival. Across experiments and temperature treatments, we found few significant CO2 effects on response traits. Survival effects were limited to a single experiment, where elevated CO2 exposure reduced embryo survival at 17 and 24 °C. Hatch length displayed CO2 × temperature interactions due largely to reduced hatch size at 24 °C in one experiment but increased length at 28 °C in another. We found no overall influence of CO2 on larval growth or survival to 9, 10, 15 and 13–22 days post-hatch, at 28, 24, 20, and 17 °C, respectively. Importantly, exposure to cooler (17 °C) and warmer (28 °C) than optimal rearing temperatures (24 °C) in this species did not appear to increase CO2 sensitivity. Repeated experimentation documented substantial inter- and intra-experiment variability, highlighting the need for experimental replication to more robustly constrain inherently variable responses. Taken together, these results demonstrate that the early life stages of this ecologically important forage fish appear largely tolerate to even extreme levels of CO2 across a broad thermal regime. 

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3. Robust quantification of fish early life CO ₂ sensitivities via serial experimentation

   https://doi.org/10.1098/rsbl.2018.0408  

   Baumann, Hannes; Cross, Emma L.; Murray, Chris S. (November 2018, Biology Letters)

   null (Ed.)

   Despite the remarkable expansion of laboratory studies, robust estimates of single species CO 2 sensitivities remain largely elusive. We conducted a meta-analysis of 20 CO 2 exposure experiments conducted over 6 years on offspring of wild Atlantic silversides ( Menidia menidia ) to robustly constrain CO 2 effects on early life survival and growth. We conclude that early stages of this species are generally tolerant to CO 2 levels of approximately 2000 µatm, likely because they already experience these conditions on diel to seasonal timescales. Still, high CO 2 conditions measurably reduced fitness in this species by significantly decreasing average embryo survival (−9%) and embryo+larval survival (−13%). Survival traits had much larger coefficients of variation (greater than 30%) than larval length or growth (3–11%). CO 2 sensitivities varied seasonally and were highest at the beginning and end of the species' spawning season (April–July), likely due to the combined effects of transgenerational plasticity and maternal provisioning. Our analyses suggest that serial experimentation is a powerful, yet underused tool for robustly estimating small but true CO 2 effects in fish early life stages. 

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4. Fluid preservation causes minimal reduction of parasite detectability in fish specimens: A new approach for reconstructing parasite communities of the past?

   https://doi.org/10.1002/ece3.6379  

   Fiorenza, Evan A.; Leslie, Katie L.; Torchin, Mark E.; Maslenikov, Katherine P.; Tornabene, Luke; Wood, Chelsea L. (June 2020, Ecology and Evolution)

   Abstract Long‐term datasets are needed to evaluate temporal patterns in wildlife disease burdens, but historical data on parasite abundance are extremely rare. For more than a century, natural history collections have been accumulating fluid‐preserved specimens, which should contain the parasites infecting the host at the time of its preservation. However, before this unique data source can be exploited, we must identify the artifacts that are introduced by the preservation process. Here, we experimentally address whether the preservation process alters the degree to which metazoan parasites are detectable in fluid‐preserved fish specimens when using visual parasite detection techniques. We randomly assigned fish of three species (Gadus chalcogrammus, Thaleichthys pacificus, and Parophrys vetulus) to two treatments. In the first treatment, fish were preserved according to the standard procedures used in ichthyological collections. Immediately after the fluid‐preservation process was complete, we performed parasitological dissection on those specimens. The second treatment was a control, in which fish were dissected without being subjected to the fluid‐preservation process. We compared parasite abundance between the two treatments. Across 298 fish individuals and 59 host–parasite pairs, we found few differences between treatments, with 24 of 27 host–parasite pairs equally abundant between the two treatments. Of these, one pair was significantly more abundant in the preservation treatment than in the control group, and two pairs were significantly less abundant in the preservation treatment than in the control group. Our data suggest that the fluid‐preservation process does not have a substantial effect on the detectability of metazoan parasites. This study addresses only the effects of the fixation and preservation process; long‐term experiments are needed to address whether parasite detectability remains unchanged in the months, years, and decades of storage following preservation. If so, ecologists will be able to reconstruct novel, long‐term datasets on parasite diversity and abundance over the past century or more using fluid‐preserved specimens from natural history collections. 

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5. Comparing therapeutic modulators of the SOD1 G93A Amyotrophic Lateral Sclerosis mouse pathophysiology

   https://doi.org/10.3389/fnins.2022.1111763  

   Lee, Albert J.; Kittel, Tyler E.; Kim, Renaid B.; Bach, Thao-Nguyen; Zhang, Tian; Mitchell, Cassie S. (January 2023, Frontiers in Neuroscience)

   Introduction Amyotrophic Lateral Sclerosis (ALS) is a paralyzing, multifactorial neurodegenerative disease with limited therapeutics and no known cure. The study goal was to determine which pathophysiological treatment targets appear most beneficial. Methods A big data approach was used to analyze high copy SOD1 G93A experimental data. The secondary data set comprised 227 published studies and 4,296 data points. Treatments were classified by pathophysiological target: apoptosis, axonal transport, cellular chemistry, energetics, neuron excitability, inflammation, oxidative stress, proteomics, or systemic function. Outcome assessment modalities included onset delay, health status (rotarod performance, body weight, grip strength), and survival duration. Pairwise statistical analysis (two-tailed t -test with Bonferroni correction) of normalized fold change (treatment/control) assessed significant differences in treatment efficacy. Cohen’s d quantified pathophysiological treatment category effect size compared to “all” (e.g., all pathophysiological treatment categories combined). Results Inflammation treatments were best at delaying onset ( d = 0.42, p > 0.05). Oxidative stress treatments were significantly better for prolonging survival duration ( d = 0.18, p < 0.05). Excitability treatments were significantly better for prolonging overall health status ( d = 0.22, p < 0.05). However, the absolute best pathophysiological treatment category for prolonging health status varied with disease progression: oxidative stress was best for pre-onset health ( d = 0.18, p > 0.05); excitability was best for prolonging function near onset ( d = 0.34, p < 0.05); inflammation was best for prolonging post-onset function ( d = 0.24, p > 0.05); and apoptosis was best for prolonging end-stage function ( d = 0.49, p > 0.05). Finally, combination treatments simultaneously targeting multiple pathophysiological categories (e.g., polytherapy) performed significantly ( p < 0.05) better than monotherapies at end-stage. Discussion In summary, the most effective pathophysiological treatments change as function of assessment modality and disease progression. Shifting pathophysiological treatment category efficacy with disease progression supports the homeostatic instability theory of ALS disease progression. 

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