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Seagrass meadows are globally important blue carbon sinks. In northern cold-temperate regions, eelgrass (Zostera marina) is the dominant seagrass species, and although their sedimentary carbon stocks have been quantified across regions, information regarding the CO2 withdrawal capacity as carbon sinks remains scarce. Here we assessed the carbon (Corg) accumulation rates (CARs) and stocks as well as the organic matter sources in five seagrass meadows in the Gullmar Fjord area on the Swedish Skagerrak coast. We found that the mean (±SD) CAR was 14 ± 3 g Corg m-2 yr-1 over the last ~120–140 years (corresponding to a yearly uptake of 52.4 ± 12.6 g CO2 m-2). The carbon sink capacity is in line with other Z. marina areas but relatively low compared to other seagrass species and regions globally. About half of the sedimentary carbon accumulation (7.1 ± 3.3 g Corg m-2 yr-1) originated from macroalgae biomass, which highlights the importance of non-seagrass derived material for the carbon sink function of seagrass meadows in the area. The Corg stocks were similar among sites when comparing at a standardized depth of 50 cm (4.6–5.9 kg Corg m-2), but showed large variation when assessed for the total extent of the cores (ranging from 0.7 to 20.6 kg Corg m-2 for sediment depths of 11 to at least 149 cm). The low sediment accretion rates (1.18–1.86 mm yr-1) and the relatively thick sediment deposits (with a maximum of >150 cm of sediment depth) suggests that the carbon stocks have likely been accumulated for an extended period of time, and that the documented loss of seagrass meadows in the Swedish Skagerrak region and associated erosion of the sediment could potentially have offset centuries of carbon sequestration., Funder:Albert och Maria Bergström foundationBolin Centre for climate research

[EN] The present invention relates to an activator of a gene belonging to the SA-c1 module for use in the treatment of NB malignancies in a subject, as well as to an in vitro method for designing a personalized therapy for a subject with NB malignancies., [FR] La présente invention concerne un activateur d'un gène appartenant au module SA-c1 pour une utilisation dans le traitement de malignités NB chez un sujet, ainsi qu'un procédé in vitro d'établissement d'une thérapie personnalisée pour un sujet atteint de malignités NB.

Llegar a entender cómo funciona el cerebro y cómo este interacciona con el ecosistema para interpretar el mundo que nos rodea sin duda facilitará el desarrollo de estrategias más eficaces para tratar o curar los trastornos neurológicos y psiquiátricos. Además, la comprensión de los principios fundamentales que controlan el funcionamiento del sistema nervioso transformará nuestra visión sobre muchas cuestiones que han sido tradicionalmente enmarcadas en el campo de la filosofía, repercutiendo en áreas como la economía o el derecho. Las neurociencias nos ayudarán, en definitiva, a entender qué nos hace humanos. Este es un campo en el que los investigadores del CSIC destacan internacionalmente y así debe seguir siendo en los próximos años. Para lograrlo, deberíamos potenciar y reforzar nuestras investigaciones en los ocho desafíos que describimos en este volumen.

Centrosomes are the main microtubule-organizing centres, playing essential roles in the organization of the cytoskeleton during interphase, and in the mitotic spindle, which controls chromosome segregation, during cell division. Centrosomes also act as the basal body of cilia, regulating cilium length and affecting extracellular signal reception as well as the integration of intracellular signalling pathways. Centrosomes are self-replicative and duplicate once every cell cycle to generate two centrosomes. The core support structure of the centrosome consists of two molecularly distinct centrioles. The mother (mature) centriole exhibits accessory appendages and is surrounded by both pericentriolar material and centriolar satellites, structures that the daughter (immature) centriole lacks. In this Review, we discuss what is currently known about centrosome duplication, its dialogue with the cell cycle and the sequential acquisition of specific components during centriole maturation. We also describe our current understanding of the mature centriolar structures that are required to build a cilium. Altogether, the built-in centrosome asymmetries that stem from the two centrosomes inheriting molecularly different centrioles sets the foundation for cell division being an intrinsically asymmetric process.

The study of the brain will tell us what makes us humans and how our social behavior generates. Increasing our understanding of how the brain functions and interacts with the ecosystem to interpret the world will not only help to find effective means to treat and/or cure neurological and psychiatric disorders but will also change our vision on questions pertaining to philosophy and humanities and transform other fields such as economy and law. Neurosciences research at the CSIC is already valuable and should be intensified mainly focused on the eight major challenges described in this volume.

The neural tube in amniotic embryos forms as a result of two consecutive events along the anteroposterior axis, referred to as primary and secondary neurulation (PN and SN). While PN involves the invagination of a sheet of epithelial cells, SN shapes the caudal neural tube through the mesenchymal-to-epithelial transition (MET) of neuromesodermal progenitors, followed by cavitation of the medullary cord. The technical difficulties in studying SN mainly involve the challenge of labeling and manipulating SN cells in vivo. Here we describe a new method to follow MET during SN in the chick embryo, combining early in ovo chick electroporation with in vivo time-lapse imaging. This procedure allows the cells undergoing SN to be manipulated in order to investigate the MET process, permitting their cell dynamics to be followed in vivo.

Class II HLH proteins heterodimerize with class I HLH/E proteins to regulate transcription. Here, we show that E proteins sharpen neurogenesis by adjusting the neurogenic strength of the distinct proneural proteins. We find that inhibiting BMP signaling or its target ID2 in the chick embryo spinal cord, impairs the neuronal production from progenitors expressing ATOH1/ASCL1, but less severely that from progenitors expressing NEUROG1/2/PTF1a. We show this context-dependent response to result from the differential modulation of proneural proteins’ activity by E proteins. E proteins synergize with proneural proteins when acting on CAGSTG motifs, thereby facilitating the activity of ASCL1/ATOH1 which preferentially bind to such motifs. Conversely, E proteins restrict the neurogenic strength of NEUROG1/2 by directly inhibiting their preferential binding to CADATG motifs. Since we find this mechanism to be conserved in corticogenesis, we propose this differential co-operation of E proteins with proneural proteins as a novel though general feature of their mechanism of action.

Zika virus (ZikV) is a flavivirus that infects neural tissues, causing congenital microcephaly. ZikV has evolved multiple mechanisms to restrict proliferation and enhance cell death, although the underlying cellular events involved remain unclear. Here we show that the ZikV-NS5 protein interacts with host proteins at the base of the primary cilia in neural progenitor cells, causing an atypical non-genetic ciliopathy and premature neuron delamination. Furthermore, in human microcephalic fetal brain tissue, ZikV-NS5 persists at the base of the motile cilia in ependymal cells, which also exhibit a severe ciliopathy. Although the enzymatic activity of ZikV-NS5 appears to be dispensable, the amino acids Y25, K28, and K29 that are involved in NS5 oligomerization are essential for localization and interaction with components of the cilium base, promoting ciliopathy and premature neurogenesis. These findings lay the foundation for therapies that target ZikV-NS5 multimerization and prevent the developmental malformations associated with congenital Zika syndrome.

The growth and evolutionary expansion of the cerebral cortex are defined by the spatial-temporal production of neurons, which itself depends on the decision of radial glial cells (RGCs) to self-amplify or to switch to neurogenic divisions. The mechanisms regulating these RGC fate decisions are still incompletely understood. Here, we describe a novel and evolutionarily conserved role of the canonical BMP transcription factors SMAD1/5 in controlling neurogenesis and growth during corticogenesis. Reducing the expression of both SMAD1 and SMAD5 in neural progenitors at early mouse cortical development caused microcephaly and an increased production of early-born cortical neurons at the expense of late-born ones, which correlated with the premature differentiation and depletion of the pool of cortical progenitors. Gain- and loss-of-function experiments performed during early cortical neurogenesis in the chick revealed that SMAD1/5 activity supports self-amplifying RGC divisions and restrains the neurogenic ones. Furthermore, we demonstrate that SMAD1/5 stimulate RGC self-amplification through the positive post-transcriptional regulation of the Hippo signalling effector YAP. We anticipate this SMAD1/5-YAP signalling module to be fundamental in controlling growth and evolution of the amniote cerebral cortex.

The generation of organoids is one of the biggest scientific advances in regenerative medicine. Here, by lengthening the time that human pluripotent stem cells (hPSCs) were exposed to a three-dimensional microenvironment, and by applying defined renal inductive signals, we generated kidney organoids that transcriptomically matched second-trimester human fetal kidneys. We validated these results using ex vivo and in vitro assays that model renal development. Furthermore, we developed a transplantation method that utilizes the chick chorioallantoic membrane. This approach created a soft in vivo microenvironment that promoted the growth and differentiation of implanted kidney organoids, as well as providing a vascular component. The stiffness of the in ovo chorioallantoic membrane microenvironment was recapitulated in vitro by fabricating compliant hydrogels. These biomaterials promoted the efficient generation of renal vesicles and nephron structures, demonstrating that a soft environment accelerates the differentiation of hPSC-derived kidney organoids.

Global patterns of planktonic diversity are mainly determined by the dispersal of propagules with ocean currents. However, the role that abundance and body size play in determining spatial patterns of diversity remains unclear. Here we analyse spatial community structure - beta-diversity - for several planktonic and nektonic organisms from prokaryotes to small mesopelagic fishes collected during the Malaspina 2010 Expedition. beta-diversity was compared to surface ocean transit times derived from a global circulation model, revealing a significant negative relationship that is stronger than environmental differences. Estimated dispersal scales for different groups show a negative correlation with body size, where less abundant large-bodied communities have significantly shorter dispersal scales and larger species spatial turnover rates than more abundant small-bodied plankton. Our results confirm that the dispersal scale of planktonic and micro-nektonic organisms is determined by local abundance, which scales with body size, ultimately setting global spatial patterns of diversity.

Embryonic development of the central nervous system (CNS) requires the proliferation of neural progenitor cells to be tightly regulated, allowing the formation of an organ with the right size and shape. This includes regulation of both the spatial distribution of mitosis and the mode of cell division. The centrosome, which is the main microtubule-organizing centre of animal cells, contributes to both of these processes. Here, we discuss the impact that centrosome-mediated control of cell division has on the shape of the overall growing CNS. We also review the intrinsic properties of the centrosome, both in terms of its molecular composition and its signalling capabilities, and discuss the fascinating notion that intrinsic centrosomal asymmetries in dividing neural progenitor cells are instructive for neurogenesis. Finally, we discuss the genetic links between centrosome dysfunction during development and the aetiology of microcephaly.

Tight control of the balance between self-expanding symmetric and self-renewing asymmetric neural progenitor divisions is crucial to regulate the number of cells in the developing central nervous system. We recently demonstrated that Sonic hedgehog (Shh) signalling is required for the expansion of motor neuron progenitors by maintaining symmetric divisions. Here we show that activation of Shh/Gli signalling in dividing neuroepithelial cells controls the symmetric recruitment of PKA to the centrosomes that nucleate the mitotic spindle, maintaining symmetric proliferative divisions. Notably, Shh signalling upregulates the expression of pericentrin, which is required to dock PKA to the centrosomes, which in turn exerts a positive feedback onto Shh signalling. Thus, by controlling centrosomal protein assembly, we propose that Shh signalling overcomes the intrinsic asymmetry at the centrosome during neuroepithelial cell division, thereby promoting self-expanding symmetric divisions and the expansion of the progenitor pool.