The Habitats and Biodiversity of Watamu Marine National Park: Evaluating Our Knowledge of One of East Africa's Oldest Marine Protected Areas

Watamu Marine National Park (WMNP) is one of the oldest no-take Marine Protected Areas (MPAs) in the world. Since its establishment in 1968, it has been the subject of a number of scientific studies as well as suffering from a range of modern threats to coastal marine habitats. The current state and conservation value of WMNP is documented in terms of habitat, biodiversity, and available scientific literature. There were 101 published references relating to WMNP found, which mostly focus on coral reef ecology, with less attention to other topics, such as biodiversity, socio-economics, or the ecology of non-coral reef habitats. The habitat map produced of WMNP is the first to show this level of detail and the only habitat map of a Kenyan MPA. Nine habitat categories were mapped; revealing that the most dominant habitat type is seagrass and the least is coral reef. Species lists were collected for fish, echinoderms, molluscs, crustaceans, corals, and seagrass, and species abundances were used to estimate total species richness, species diversity and sampling completeness. There were 18 species across all groups that fall into a category of conservation concern (other than Least Concern or Not Evaluated) on the IUCN Red List and 8 species found which are currently undescribed. The findings of this paper emphasise the importance of non-coral habitats in the WMNP, such as seagrass beds, and the need for more research into the ecology and conservation importance of these habitats. The information provided in this paper provides a comprehensive overview to any scientist or conservationist wanting to carry out further work in WMNP

Kif13b Regulates PNS and CNS Myelination Through the Dlg1 Scaffold

Microtubule-based kinesin motors have many cellular functions, including the transport of a variety of cargos. However, unconventional roles have recently emerged, and kinesins have also been reported to act as scaffolding proteins and signaling molecules. In this work, we further extend the notion of unconventional functions for kinesin motor proteins, and we propose that Kif13b kinesin acts as a signaling molecule regulating peripheral nervous system (PNS) and central nervous system (CNS) myelination. In this process, positive and negative signals must be tightly coordinated in time and space to orchestrate myelin biogenesis. Here, we report that in Schwann cells Kif13b positively regulates myelination by promoting p38γ mitogen-activated protein kinase (MAPK)-mediated phosphorylation and ubiquitination of Discs large 1 (Dlg1), a known brake on myelination, which downregulates the phosphatidylinositol 3-kinase (PI3K)/v-AKT murine thymoma viral oncogene homolog (AKT) pathway. Interestingly, Kif13b also negatively regulates Dlg1 stability in oligodendrocytes, in which Dlg1, in contrast to Schwann cells, enhances AKT activation and promotes myelination. Thus, our data indicate that Kif13b is a negative regulator of CNS myelination. In summary, we propose a novel function for the Kif13b kinesin in glial cells as a key component of the PI3K/AKT signaling pathway, which controls myelination in both PNS and CNS

Revisiting adult neurogenesis and the role of erythropoietin for neuronal and oligodendroglial differentiation in the hippocampus

Recombinant human erythropoietin (EPO) improves cognitive performance in neuropsychiatric diseases ranging from schizophrenia and multiple sclerosis to major depression and bipolar disease. This consistent EPO effect on cognition is independent of its role in hematopoiesis. The cellular mechanisms of action in brain, however, have remained unclear. Here we studied healthy young mice and observed that 3-week EPO administration was associated with an increased number of pyramidal neurons and oligodendrocytes in the hippocampus of similar to 20%. Under constant cognitive challenge, neuron numbers remained elevated until >6 months of age. Surprisingly, this increase occurred in absence of altered cell proliferation or apoptosis. After feeding a $^{15}$N-leucine diet, we used nanoscopic secondary ion mass spectrometry, and found that in EPO-treated mice, an equivalent number of neurons was defined by elevated $^{15}$N-leucine incorporation. In EPO-treated NG2-Cre-ERT2 mice, we confirmed enhanced differentiation of preexisting oligodendrocyte precursors in the absence of elevated DNA synthesis. A corresponding analysis of the neuronal lineage awaits the identification of suitable neuronal markers. In cultured neurospheres, EPO reduced Sox9 and stimulated miR124, associated with advanced neuronal differentiation. We are discussing a resulting working model in which EPO drives the differentiation of non-dividing precursors in both (NG2+) oligodendroglial and neuronal lineages. As endogenous EPO expression is induced by brain injury, such a mechanism of adult neurogenesis may be relevant for central nervous system regeneration