HAS THE RECOLONIZATION OF THE PO PLAIN BEGUN? UPDATES REGARDING THE PRESENCE OF THE EURASIAN OTTER (Lutra lutra) IN NORTH-EASTERN ITALY

Widespread in Italy in the early 1900s, the Eurasian otter subsequently underwent a dramatic decline that led to its local extinction in many administrative regions, with the exception of a small residual nucleus in southern Italy. For a few years now, the Austrian and Slovenian populations adjacent to north-eastern Italy have been increasing sharply, leading to a recolonization of the area by the species. During 2020, in Friuli Venezia Giulia, surveys of signs of presence were carried out in 48 grid cells (10 x 10 km) to update information on the species’ local distribution. The following monitoring methods were used: monitoring beneath bridges combined with transects along water courses. 17 grid cells tested positive for the presence of the species, and currently, the otter appears widely distributed in Friuli Venezia Giulia along the main waterways of the Eastern Alps and Prealps, and in some areas overlooking the plain of the Tagliamento and the transborder Isonzo-Soča basin, both included in the Po plain. These constitute the first observations of the species for more than 50 years. Compared to previous studies, 13 new grid cells involving the presence of otters were identified, including in lowland areas, suggesting a progressive expansion from the mountain ranges towards the Po-Venetian Plain. This represents, a spur to expand research and implement new studies to improve levels of knowledge about and the consequent protection of the species. Finally, the integration of transects along riverbanks to monitoring beneath bridges, allowed us both to collect numerous observation and to compare our results with previous studies

Analysing the performance of MCECs over a wide range of operating temperatures

Hydrogen production through water electrolysis has gained significant attention in the past years as a means of tackling the problem of the imbalance between the intermittent rate of electricity production from renewable sources and the continuous electricity demand from end users. Recently, much of the effort has been shifted toward the electrolysis of steam rather than water, for example in solid oxide cells, which operate at temperatures around 800°C. In this manner, part of the energy required for the conversion to hydrogen is provided as heat rather than electricity. At the same time, the high temperature levels require the use of highly resistant materials, which increase the overall cost of the process. An interesting alternative is represented by molten carbonate electrolysis cells (MCECs), operating at temperatures well below 700°C. In the present work, a molten carbonate cell was operated in a lower temperature range (490-550°C) by changing the composition of the electrolyte mixture. The data obtained, along with experimental results at higher temperature (570-650°C) available in the literature, was analyzed using a 0D model accounting for Ohmic and activation overpotentials to determine the correlation between current and potential. It was found that, while the dependence of Ohmic losses on temperatures is discontinuous when cell operation is switched from the lower to the higher temperature range, activation losses vary with continuity. This result provides important insight on the performance of MCECs that can serve as a basis for future studies

Mutations in thyroid hormone receptor α1 cause premature neurogenesis and progenitor cell depletion in human cortical development

Mutations in the thyroid hormone receptor α 1 gene (THRA) have recently been identified as a cause of intellectual deficit in humans. Patients present with structural abnormalities including microencephaly, reduced cerebellar volume and decreased axonal density. Here, we show that directed differentiation of THRA mutant patient-derived induced pluripotent stem cells to forebrain neural progenitors is markedly reduced, but mutant progenitor cells can generate deep and upper cortical layer neurons and form functional neuronal networks. Quantitative lineage tracing shows that THRA mutation-containing progenitor cells exit the cell cycle prematurely, resulting in reduced clonal output. Using a micropatterned chip assay, we find that spatial self-organization of mutation-containing progenitor cells in vitro is impaired, consistent with down-regulated expression of cell–cell adhesion genes. These results reveal that thyroid hormone receptor α1 is required for normal neural progenitor cell proliferation in human cerebral cortical development. They also exemplify quantitative approaches for studying neurodevelopmental disorders using patient-derived cells in vitro

Mutations in thyroid hormone receptor α1 cause premature neurogenesis and progenitor cell depletion in human cortical development.

Mutations in the thyroid hormone receptor α 1 gene (THRA) have recently been identified as a cause of intellectual deficit in humans. Patients present with structural abnormalities including microencephaly, reduced cerebellar volume and decreased axonal density. Here, we show that directed differentiation of THRA mutant patient-derived induced pluripotent stem cells to forebrain neural progenitors is markedly reduced, but mutant progenitor cells can generate deep and upper cortical layer neurons and form functional neuronal networks. Quantitative lineage tracing shows that THRA mutation-containing progenitor cells exit the cell cycle prematurely, resulting in reduced clonal output. Using a micropatterned chip assay, we find that spatial self-organization of mutation-containing progenitor cells in vitro is impaired, consistent with down-regulated expression of cell-cell adhesion genes. These results reveal that thyroid hormone receptor α1 is required for normal neural progenitor cell proliferation in human cerebral cortical development. They also exemplify quantitative approaches for studying neurodevelopmental disorders using patient-derived cells in vitro.NIHR Cambridge Biomedical Centr

Epigenetic engineering shows that a human centromere resists silencing mediated by H3K27me3/K9me3

Centromeres are characterized by the centromere-specific H3 variant CENP-A, which is embedded in chromatin with a pattern characteristic of active transcription that is required for centromere identity. It is unclear how centromeres remain transcriptionally active despite being flanked by repressive pericentric heterochromatin. To further understand centrochromatin’s response to repressive signals, we nucleated a Polycomb-like chromatin state within the centromere of a human artificial chromosome (HAC) by tethering the methyltransferase EZH2. This led to deposition of the H3K27me3 mark and PRC1 repressor binding. Surprisingly, this state did not abolish HAC centromere function or transcription, and this apparent resistance was not observed on a noncentromeric locus, where transcription was silenced. Directly tethering the reader/repressor PRC1 bypassed this resistance, inactivating the centromere. We observed analogous responses when tethering the heterochromatin Editor Suv39h1-methyltransferase domain (centromere resistance) or reader HP1α (centromere inactivation), respectively. Our results reveal that the HAC centromere can resist repressive pathways driven by H3K9me3/H3K27me3 and may help to explain how centromeres are able to resist inactivation by flanking heterochromatin