Spawning fish maintains trophic synchrony across time and space beyond thermal drivers.

Increasing ocean temperature will speed up physiological rates of ectotherms. In fish, this is suggested to cause earlier spawning due to faster oocyte growth rates. Over time, this could cause spawning time to become decoupled from the timing of offspring food resources, a phenomenon referred to as trophic asynchrony. We used biological data, including body length, age, and gonad developmental stages collected from >125,000 individual Northeast Arctic cod (Gadus morhua) sampled between 59 and 73° N in 1980-2019. Combined with experimental data on oocyte growth rates, our analyses show that cod spawned progressively earlier by about a week per decade, partly due to ocean warming. It also appears that spawning time varied by more than 40 days, depending on year and spawning location. The significant plasticity in spawning time seems to be fine-tuned to the local phytoplankton spring bloom phenology. This ability to partly overcome thermal drivers and thus modulate spawning time could allow individuals to maximize fitness by closely tracking local environmental conditions important for offspring survival. Our finding highlights a new dimension for trophic match-mismatch and should be an important consideration in models used to predict phenology dynamics in a warmer climate.

Land use change and coastal water darkening drive synchronous dynamics in phytoplankton and fish phenology on centennial timescales.

At high latitudes, the suitable window for timing reproductive events is particularly narrow, promoting tight synchrony between trophic levels. Climate change may disrupt this synchrony due to diverging responses to temperature between, for example, the early life stages of higher trophic levels and their food resources. Evidence for this is equivocal, and the role of compensatory mechanisms is poorly understood. Here, we show how a combination of ocean warming and coastal water darkening drive long-term changes in phytoplankton spring bloom timing in Lofoten Norway, and how spawning time of Northeast Arctic cod responds in synchrony. Spring bloom timing was derived from hydrographical observations dating back to 1936, while cod spawning time was estimated from weekly fisheries catch and roe landing data since 1877. Our results suggest that land use change and freshwater run-off causing coastal water darkening has gradually delayed the spring bloom up to the late 1980s after which ocean warming has caused it to advance. The cod appear to track phytoplankton dynamics by timing gonadal development and spawning to maximize overlap between offspring hatch date and predicted resource availability. This finding emphasises the importance of land-ocean coupling for coastal ecosystem functioning, and the potential for fish to adapt through phenotypic plasticity.

Centennial decline in North Sea water clarity causes strong delay in phytoplankton bloom timing.

With climate warming, a widespread expectation is that events in spring, such as flowering, bird migrations, and insect bursts, will occur earlier because of increasing temperature. At high latitudes, increased ocean temperature is suggested to advance the spring phytoplankton bloom due to earlier stabilization of the water column. However, climate warming is also expected to cause browning in lakes and rivers due to increases in terrestrial greening, ultimately reducing water clarity in coastal areas where freshwater drain. In shallow areas, decreased retention of sediments on the seabed will add to this effect. Both browning and resuspension of sediments imply a reduction of the euphotic zone and Sverdrup's critical depth leading to a delay in the spring bloom, counteracting the effect of increasing temperature. Here, we provide evidence that such a transparency reduction has already taken place in both the deep and shallow areas of the North Sea during the 20th century. A sensitivity analysis using a water column model suggests that the reduced transparency might have caused up to 3 weeks delay in the spring bloom over the last century. This delay stands in contrast to the earlier bloom onset expected from global warming, thus highlighting the importance of including changing water transparency in analyses of phytoplankton phenology and primary production. This appears to be of particular relevance for coastal waters, where increased concentrations of absorbing and scattering substances (sediments, dissolved organic matter) have been suggested to lead to coastal darkening.

Effects of growth rate, cell size, motion, and elemental stoichiometry on nutrient transport kinetics.

Nutrient acquisition is a critical determinant for the competitive advantage for auto- and osmohetero- trophs alike. Nutrient limited growth is commonly described on a whole cell basis through reference to a maximum growth rate (Gmax) and a half-saturation constant (KG). This empirical application of a Michaelis-Menten like description ignores the multiple underlying feedbacks between physiology contributing to growth, cell size, elemental stoichiometry and cell motion. Here we explore these relationships with reference to the kinetics of the nutrient transporter protein, the transporter rate density at the cell surface (TRD; potential transport rate per unit plasma-membrane area), and diffusion gradients. While the half saturation value for the limiting nutrient increases rapidly with cell size, significant mitigation is afforded by cell motion (swimming or sedimentation), and by decreasing the cellular carbon density. There is thus potential for high vacuolation and high sedimentation rates in diatoms to significantly decrease KG and increase species competitive advantage. Our results also suggest that Gmax for larger non-diatom protists may be constrained by rates of nutrient transport. For a given carbon density, cell size and TRD, the value of Gmax/KG remains constant. This implies that species or strains with a lower Gmax might coincidentally have a competitive advantage under nutrient limited conditions as they also express lower values of KG. The ability of cells to modulate the TRD according to their nutritional status, and hence change the instantaneous maximum transport rate, has a very marked effect upon transport and growth kinetics. Analyses and dynamic models that do not consider such modulation will inevitably fail to properly reflect competitive advantage in nutrient acquisition. This has important implications for the accurate representation and predictive capabilities of model applications, in particular in a changing environment.

Dynamics of phytoplankton blooms in turbulent vortex cells.

Turbulence and coherent circulation structures, such as submesoscale and mesoscale eddies, convective plumes and Langmuir cells, play a critical role in shaping phytoplankton spatial distribution and population dynamics. We use a framework of advection-reaction-diffusion equations to investigate the effects of turbulent transport on the phytoplankton population growth and its spatial structure in a vertical two-dimensional vortex flow field. In particular, we focus on how turbulent flow velocities and sinking influence phytoplankton growth and biomass aggregation. Our results indicate that conditions in mixing and growth of phytoplankton can drive different vertical spatial structures in the mixed layer, with the depth of the mixed layer being a critical factor to allow coexistence of populations with different sinking speed. With increasing mixed layer depth, positive growth for sinking phytoplankton can be maintained with increasing turbulent flow velocities, allowing the apparently counter-intuitive persistence of fast sinking phytoplankton populations in highly turbulent and deep mixed layers. These dynamics demonstrate the role of considering advective transport within a turbulent vortex and can help to explain observed phytoplankton biomass during winter in the North Atlantic, where the overturn of deep convection has been suggested to play a critical role in phytoplankton survival.

Size structures sensory hierarchy in ocean life.

Survival in aquatic environments requires organisms to have effective means of collecting information from their surroundings through various sensing strategies. In this study, we explore how sensing mode and range depend on body size. We find a hierarchy of sensing modes determined by body size. With increasing body size, a larger battery of modes becomes available (chemosensing, mechanosensing, vision, hearing and echolocation, in that order) while the sensing range also increases. This size-dependent hierarchy and the transitions between primary sensory modes are explained on the grounds of limiting factors set by physiology and the physical laws governing signal generation, transmission and reception. We theoretically predict the body size limits for various sensory modes, which align well with size ranges found in literature. The treatise of all ocean life, from unicellular organisms to whales, demonstrates how body size determines available sensing modes, and thereby acts as a major structuring factor of aquatic life.

Transcranial sonography findings in welding-related Parkinsonism in comparison to Parkinson's disease.

The pathogenetic relationship of welding-related Parkinsonism (WP) and idiopathic Parkinson's disease (PD) is a matter of debate. In the present study, we compared transcranial sonography (TCS) findings in patients with WP and PD. Two male patients with WP, who had developed levodopa-resistant akinetic-rigid Parkinsonism without ongoing progression after having worked as welders for many years in Chilean mines in confined spaces without adequate ventilation, and three age-matched male patients with clinically definite akinetic-rigid PD were studied with TCS in a random order by two investigators blind to clinical diagnoses. In both WP patients, normal echogenicity of substantia nigra was found whereas all PD patients exhibited marked substantia nigra hyperechogenicity, previously reported as a characteristic TCS finding in idiopathic PD. In contrast, lenticular nucleus was hyperechogenic in both WP patients but only in one of the PD patients. TCS findings suggest a different pathophysiology of Parkinsonism in WP and PD patients.