Patterns and drivers of macroalgal 'blue carbon' transport and deposition in near-shore coastal environments.

The role of macroalgae (seaweed) as a global contributor to carbon drawdown within marine sediments - termed 'blue carbon' - remains uncertain and controversial. While studies are needed to validate the potential for macroalgal­carbon sequestration in marine and coastal sediments, fundamental questions regarding the fate of dislodged macroalgal biomass need to be addressed. Evidence suggests macroalgal biomass may be advected and deposited within other vegetated coastal ecosystems and down to the deep ocean; however, contributions to near-shore sediments within coastal waters remain uncertain. In this study a combination of eDNA metabarcoding and surficial sediment sampling informed by seabed mapping from different physical environments was used to test for the presence of macroalgal carbon in near-shore coastal sediments in south-eastern Australia, and the physical factors influencing patterns of macroalgal transport and deposition. DNA products for a total of 68 macroalgal taxa, representing all major macroalgal groups (Phaeophyceae, Rhodophyta, and Chlorophyta) were successfully detected at 112 near-shore locations. These findings confirm the potential for macroalgal biomass to be exported into near-shore sediments and suggest macroalgal carbon donors could be both speciose and diverse. Modelling suggested that macroalgal transport and deposition, and total organic carbon (TOC), are influenced by complex interactions between several physical environmental factors including water depth, sediment grain size, wave orbital velocity, current speed, current direction, and the extent of the infralittoral zone around depositional areas. Extrapolation of the optimised model was used to predict spatial patterns of macroalgal deposition and TOC across the coastline and to identify potentially important carbon sinks. This study builds on recent studies providing empirical evidence for macroalgal biomass deposits in near-shore sediments, and a framework for predicting the spatial distribution of potential carbon sinks and informing future surveys aimed at determining the potential for long-term macroalgal carbon sequestration in marine sediments.

Detecting marine pests using environmental DNA and biophysical models.

The spread of marine pests is occurring at record rates due to globalisation and increasing trade. Environmental DNA (eDNA) is an emerging tool for pest surveillance, allowing for the detection of genetic material shed by organisms into the environment. However, factors influencing the spatial and temporal detection limits of eDNA in marine environments are poorly understood. In this study we use eDNA assays to assess the invasive ranges of two marine pests in south-eastern Australia, the kelp Undaria pinnatifida and the seastar Asterias amurensis. We explored the temporal and spatial detection limits of eDNA under different oceanographic conditions by combining estimates of eDNA decay with biophysical modelling. Positive eDNA detections at several new locations indicate the invasive range of both pest species is likely to be wider than currently assumed. Environmental DNA decay rates were similar for both species, with a decay rate constant of 0.035 h-1 for U. pinnatifida, and a decay rate constant of 0.041 h-1 for A. amurensis, resulting in a 57-73% decrease in eDNA concentrations in the first 24 h and decaying beyond the limits of detection after 3-4 days. Biophysical models informed by eDNA decay profiles indicate passive transport of eDNA up to a maximum of 10 to 20 km from its source, with a ~90-95% reduction in eDNA concentration within 1-3 km from the source, depending on local oceanography. These models suggest eDNA signals are likely to be highly localised, even in complex marine environments. This was confirmed with spatially replicated eDNA sampling around an established U. pinnatifida population indicating detection limits of ~750 m from the source. This study highlights the value of eDNA methods for marine pest surveillance and provides a much-needed description of the spatio-temporal detection limits of eDNA under different oceanographic conditions.

Pathogenesis of spinal cord injury induced edema and neuropathic pain: expression of multiple isoforms of wnk1.

BACKGROUND: Neuropathic pain (NP) is a common occurrence following spinal cord injury (SCI). Identification of specific molecular pathways that are involved in pain syndromes has become a major priority in current SCI research. We have investigated the role of a cation-dependent chloride transporter, Cl-regulatory protein Na(+)-K(+)-Cl(-) 1 (NKCC1), phosphorylation profile of NKCC1 and its specific involvement in neuropathic pain following contusion SCI (cSCI) using a rat model. Administration of the NKCC1 inhibitor bumetanide (BU) increases the mean hindpaw withdrawal latency time (WLT), thermal hyperalgesia (TH) following cSCI. These results demonstrate implication of NKCC1 co-transporter and BUin SCI-induced neuropathic pain. The with-no-lysine (K)-1 (WNK1) kinase has been shown to be an important regulator of NKCC1 phosphorylation in many systems, including nocioception. Mutations in a neuronal-specific exon of WNK1 (HSN2) was identified in patients that have hereditary sensory neuropathy type II (HSANII) also implicates WNK1 in nocioception, such that these patients have loss of perception to pain, touch and heat. In our ongoing research we proposed two studies utilizing our contusion SCI (cSCI) NP model of rat. PURPOSE: Study 1 aimed at NKCC1 expression and activity is up-regulated following cSCI in the early edema and chronic neuropathic pain phases. Study 2 aimed at identifying the expression profile of alternatively spliced WNK1 isoforms in animals exhibiting thermal hyperalgesia (TH) following cSCI. METHODS: Adult male Sprague Dawley rats (275-300 g) following laminectomy received cSCI at T9 with the NYU impactor-device II by dropping 10 g weight from the height of 12.5 mm. Control rats obtained laminectomy but no impaction. Following injury, functional recovery was assessed by BBB locomotor scores on day 1, 7, 14, 21, 35, and 42 and development of thermal hyperalgesia on day 21, 28, 35, and 42 day of injury by monitoring hind paw withdraw latency time (WLT) in seconds compared with the baseline data before injury. RESULTS: Increased NKCC1 may explain observed increase in magnetic resonance imaging (MRI) T2, exhibiting NKCC1 localization in neurons. This data supports NKCC1's role in the pathogenesis of acute and chronic phases of injury, namely spinal cord edema and chronic phase neuropathic pain. NKCC1 dependent chloride influx requires the phosphorylation at specific residues. Probing for the HSN2 exon of WNK1 reveals two key findings: i) the HSN2 exon is found in alternatively spliced neuronal isoforms found at 250 kDa and 230 kDa; ii) the 250 kDa isoform is found only in tissue that is injured. CONCLUSIONS: This data implicates the NKCC1/WNK1/WNK1HSN2 involvement in post-injury response that contributes to the development of neuropathic pain. Targeting this system may have therapeutic benefit.