Keeping Humans in the Ecosystem

The World Ocean presents many opportunities, with the blue economy projected to at least double in the next two decades. However, capitalizing on these opportunities presents significant challenges and a multi-sectoral, integrated approach to managing marine socio-ecological systems will be required to achieve the full benefits projected for the blue economy. Integrated ecosystem assessments have been identified as the best means of delivering the information upon which marine resource management decisions can be made. By their nature, these assessments are inter-disciplinary, but to date have mostly focused on the natural sciences. Inclusion of human dimensions into integrated ecosystem assessments has been lagging, but is fundamental. Here we report on a Symposium, and the articles emmanating from it that are included in this Theme Set, that address how to more effectively include human dimensions into integrated ecosystem assessments. We provide an introduction to each of the main symposium topics (governance, scenarios, indicators, participatory processes, and case studies), highlight the works that emerged from the symposium, and identify key areas in which more work is required. There is still a long way to go before we see end-to-end integrated ecosystem assessments inclusive of all the major current and potential ocean use sectors that also encompass multiple aspects of human dimensions. Nonetheless, it is also clear that progress is being made and we are developing tools and approaches, including the human dimension, that can inform management and position us to take advantage of the multi-sectoral opportunities of sustainable blue growth

Kinetic Mechanism of Myosin IXB and the Contributions of Two Class IX-specific Regions

Myosin IXb (Myo9b) was reported to be a single-headed, processive myosin. In its head domain it contains an N-terminal extension and a large loop 2 insertion that are specific for class IX myosins. We characterized the kinetic properties of purified, recombinant rat Myo9b, and we compared them with those of Myo9b mutants that had either the N-terminal extension or the loop 2 insertion deleted. Unlike other processive myosins, Myo9b exhibited a low affinity for ADP, and ADP release was not rate-limiting in the ATPase cycle. Myo9b is the first myosin for which ATP hydrolysis or an isomerization step after ATP binding is rate-limiting. Myo9b-ATP appeared to be in a conformation with a weak affinity for actin as determined by pyrene-actin fluorescence. However, in actin cosedimentation experiments, a subpopulation of Myo9b-ATP bound F-actin with a remarkably high affinity. Deletion of the N-terminal extension reduced actin affinity and increased the rate of nucleotide binding. Deletion of the loop 2 insertion reduced the actin affinity and altered the communication between actin and nucleotide-binding sites

Oxidative Stress Promotes Peroxiredoxin Hyperoxidation and Attenuates Pro-survival Signaling in Aging Chondrocytes

Oxidative stress-mediated post-translational modifications of redox-sensitive proteins are postulated as a key mechanism underlying age-related cellular dysfunction and disease progression. Peroxiredoxins (PRX) are critical intracellular antioxidants that also regulate redox signaling events. Age-related osteoarthritis is a common form of arthritis that has been associated with mitochondrial dysfunction and oxidative stress. The objective of this study was to determine the effect of aging and oxidative stress on chondrocyte intracellular signaling, with a specific focus on oxidation of cytosolic PRX2 and mitochondrial PRX3. Menadione was used as a model to induce cellular oxidative stress. Compared with chondrocytes isolated from young adult humans, chondrocytes from older adults exhibited higher levels of PRX1–3 hyperoxidation basally and under conditions of oxidative stress. Peroxiredoxin hyperoxidation was associated with inhibition of pro-survival Akt signaling and stimulation of pro-death p38 signaling. These changes were prevented in cultured human chondrocytes by adenoviral expression of catalase targeted to the mitochondria (MCAT) and in cartilage explants from MCAT transgenic mice. Peroxiredoxin hyperoxidation was observed in situ in human cartilage sections from older adults and in osteoarthritic cartilage. MCAT transgenic mice exhibited less age-related osteoarthritis. These findings demonstrate that age-related oxidative stress can disrupt normal physiological signaling and contribute to osteoarthritis and suggest peroxiredoxin hyperoxidation as a potential mechanism