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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 posttranscriptional 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. [ABSTRACT FROM AUTHOR]

The subtropical ocean gyres are recognized as great marine accummulation zones of floating plastic debris; however, the possibility of plastic accumulation at polar latitudes has been overlooked because of the lack of nearby pollution sources. In the present study, the Arctic Ocean was extensively sampled for floating plastic debris from the Tara Oceans circumpolar expedition. Although plastic debris was scarce or absent in most of the Arctic waters, it reached high concentrations (hundreds of thousands of pieces per square kilometer) in the northernmost and easternmost areas of the Greenland and Barents seas. The fragmentation and typology of the plastic suggested an abundant presence of aged debris that originated from distant sources. This hypothesis was corroborated by the relatively high ratios of marine surface plastic to local pollution sources. Surface circulation models and field data showed that the poleward branch of the Thermohaline Circulation transfers floating debris from the North Atlantic to the Greenland and Barents seas, which would be a dead end for this plastic conveyor belt. Given the limited surface transport of the plastic that accumulated here and the mechanisms acting for the downward transport, the seafloor beneath this Arctic sector is hypothesized as an important sink of plastic debris.

The transforming growth factor beta (TGF-β) pathway plays key roles in development and cancer. TGF-β signaling converges on the Smad2 and Smad3 effectors, which can either cooperate or antagonize to regulate their transcriptional targets. Here we performed in vivo and in silico experiments to study how such cooperativity and antagonism might function during neurogenesis. In vivo electroporation experiments in the chick embryo neural tube show that Smad2 and Smad3 cooperate to promote neurogenesis, as well as the transcription of Smad3-specific targets. Knockdown of Smad2 enhances neurogenesis and the transcription of Smad3-specific targets. A mathematical model of the TGF-β pathway fits the experimental results and predicts that the proportions of the three different trimeric complexes formed dictates the transcriptional responses of the R-Smad proteins. As such, Smad2 targets are activated solely by the Smad2-Smad2-Smad4 complex, whereas Smad3 targets are activated both by Smad2-Smad3-Smad4 and Smad3-Smad3-Smad4 trimers. We have modeled the Smad responses onto arbitrary genes and propose that this mechanism might be extended to additional activities of TGF-β in development and disease. [ABSTRACT FROM AUTHOR]