Nature is a rich source of medicine - if we can protect it

First paragraph: The Pacific yew tree is a fairly small and slow growing conifer native to the Pacific Northwest. The Gila monster is a lizard with striking orange and black markings from the drylands of the Southwestern US and Mexico. Two very different organisms, but with a fascinating connection. They've both given us drugs that have saved and improved the lives of millions of people. Paclitaxel, originally isolated in 1971 from the bark of the Pacific Yew tree, is so important for treating various cancers that it is one of the World Health Organisation’s "Essential Medicines". This compound has been studied in more than 3,000 clinical trials. It's safe and effective and it generates sales of around US$80-100m per year.https://theconversation.com/nature-is-a-rich-source-of-medicine-if-we-can-protect-it-10747

La naturaleza es un filón para obtener medicinas, pero solo si la protegemos

First paragraph: El Taxus brevifolia, comúnmente conocido como Tejo del Pacífico, es una conífera de tamaño reducido y de crecimiento lento originaria del Pacífico Noroeste. El monstruo de Gila es un lagarto que tiene unas llamativas marcas naranjas y negras que habita las áridas tierras del suroeste de Estados Unidos y México. Son dos organismos muy diferentes pero que comparten una conexión fascinante. Ambos nos han proporcionado medicamentos que han salvado y mejorado las vidas de millones de personas.Translation of Piper R, Kagansky A, Malone J, Bunnefeld N & Jenkins R (2018) Nature is a rich source of medicine - if we can protect it. The Conversation, 13.12.2018. https://theconversation.com/nature-is-a-rich-source-of-medicine-if-we-can-protect-it-107471 https://theconversation.com/la-naturaleza-es-un-filon-para-obtener-medicinas-pero-solo-si-la-protegemos-10893

Empowering Do-it-yourself Biology by Doing-it-together: Collective Responsibility in Maximizing Benefit and Mitigating Risk

Rapid technological advances in genome editing and synthetic biology have created an unprecedented ability for science to be conducted outside traditional research institutions. This open science movement, known as do-it-yourself biology (DIY Bio) has gained significant traction and has grown exponentially in the last decade with over 160 active groups and thousands of DIY Biologists from a range of backgrounds worldwide. As a result, the movement has become a platform for biotechnology entrepreneurship and an instrument for discovery-based science education and outreach (Kolodziejczyk 2017; Landrain et al. 2013). The COVID-19 pandemic has also further emphasised the potential positive impact that the DIY Bio community can bring towards enhancing the innovative capacity of the larger scientific enterprise. As DIY biologists and scientists from traditional institutions share experimental data and designs on various platforms including online forums in response to the current pandemic, it is becoming evident that the scientific ecosystem has much to gain by being more inclusive. However, the inherent fast-evolving, open and relatively unregulated nature of DIY Bio creates substantial safety and security concerns. Here, we discuss the benefits and risks of DIY Bio and how multiple stakeholders, especially the government and academia, might work together with the DIY Bio community to co-develop global and locally contextualized policies, regulatory frameworks and action plans for maximum benefit and minimum risk.The Global Young Academy receives its core funding from the German Federal Ministry of Education and Research, the GYA DIY Biology Working Group’s activities have been co-funded by the Volkswagen Foundation

Distinct p63 and p73 Protein Interactions Predict Specific Functions in mRNA Splicing and Polyploidy Control in Epithelia.

Epithelial organs are the first barrier against microorganisms and genotoxic stress, in which the p53 family members p63 and p73 have both overlapping and distinct functions. Intriguingly, p73 displays a very specific localization to basal epithelial cells in human tissues, while p63 is expressed in both basal and differentiated cells. Here, we analyse systematically the literature describing p63 and p73 protein-protein interactions to reveal distinct functions underlying the aforementioned distribution. We have found that p73 and p63 cooperate in the genome stability surveillance in proliferating cells; p73 specific interactors contribute to the transcriptional repression, anaphase promoting complex and spindle assembly checkpoint, whereas p63 specific interactors play roles in the regulation of mRNA processing and splicing in both proliferating and differentiated cells. Our analysis reveals the diversification of the RNA and DNA specific functions within the p53 family

Towards policies that capture the expected value of biomolecular diversity for drug discovery, human health, and well-being

This paper aims to help policy makers with a characterization of the intrinsic value of biodiversity and its role as a critical foundation for sustainable development, human health, and well-being. Our objective is to highlight the urgent need to overcome economic, disciplinary, national, cultural, and regional barriers, in order to work out innovative measures to create a sustainable future and prevent the mutual extinction of humans and other species. We emphasize the pervasive neglect paid to the cross-dependency of planetary health, the health of individual human beings and other species. It is critical that social and natural sciences are taken into account as key contributors to forming policies related to biodiversity, conservation, and health management. We are reaching the target date of Nagoya treaty signatories to have accomplished measures to prevent biodiversity loss, providing a unique opportunity for policy makers to make necessary adjustments and refocus targets for the next decade. We propose recommendations for policy makers to explore novel avenues to halt the accelerated global loss of biodiversity. Beyond the critical ecological functions biodiversity performs, its enormous untapped the repertoire of natural molecular diversity is needed for solving accelerating global healthcare challenges

Molecular mechanisms governing the stem cell's fate in brain cancer: factors of stemness and quiescence

Cellular quiescence is a reversible, non-cycling state controlled by epigenetic, transcriptional and niche-associated molecular factors. Quiescence is a condition where molecular signaling pathways maintain the poised cell-cycle state whilst enabling rapid cell cycle re-entry. To achieve therapeutic breakthroughs in oncology it is crucial to decipher these molecular mechanisms employed by the cancerous milieu to control, maintain and gear stem cells towards re-activation. Cancer stem-like cells (CSCs) have been extensively studied in most malignancies, including glioma. Here, the aberrant niche activities skew the quiescence/activation equilibrium, leading to rapid tumor relapse after surgery and/or chemotherapy. Unraveling quiescence mechanisms promises to afford prevention of (often multiple) relapses, a key problem in current glioma treatment. This review article covers the current knowledge regarding normal and aberrant cellular quiescence control whilst also exploring how different molecular mechanisms and properties of the neighboring cells can influence the molecular processes behind glioma stem cell quiescence.

Restricted epigenetic inheritance of H3K9 methylation

Post-translational histone modifications are believed to allow the epigenetic transmission of distinct chromatin states, independently of associated DNA sequences. H3K9 methylation is essential for heterochromatin formation, however, a demonstration of its epigenetic heritability is lacking. Fission yeast has a single H3K9 methyltransferase, Clr4, that directs all H3K9 methylation and heterochromatin. Utilizing releasable tethered Clr4 reveals that an active process rapidly erases H3K9 methylation from tethering sites in wild-type cells. However, inactivation of the putative histone demethylase Epe1 allows H3K9 methylation and silent chromatin maintenance at the tethering site through many mitotic divisions, and transgenerationally through meiosis, after release of tethered Clr4. Thus, H3K9 methylation is a heritable epigenetic mark whose transmission is usually countered by its active removal, which prevents the unauthorised inheritance of heterochromatin

Molecular Mechanisms Governing the Stem Cell’s Fate in Brain Cancer: Factors of Stemness and Quiescence

Cellular quiescence is a reversible, non-cycling state controlled by epigenetic, transcriptional and niche-associated molecular factors. Quiescence is a condition where molecular signaling pathways maintain the poised cell-cycle state whilst enabling rapid cell cycle re-entry. To achieve therapeutic breakthroughs in oncology it is crucial to decipher these molecular mechanisms employed by the cancerous milieu to control, maintain and gear stem cells towards re-activation. Cancer stem-like cells (CSCs) have been extensively studied in most malignancies, including glioma. Here, the aberrant niche activities skew the quiescence/activation equilibrium, leading to rapid tumor relapse after surgery and/or chemotherapy. Unraveling quiescence mechanisms promises to afford prevention of (often multiple) relapses, a key problem in current glioma treatment. This review article covers the current knowledge regarding normal and aberrant cellular quiescence control whilst also exploring how different molecular mechanisms and properties of the neighboring cells can influence the molecular processes behind glioma stem cell quiescence