Chromatin profiling of a liverwort genome reveals an epigenomic landscape where the major mark of developmental silencing in later-branching land plants and in animals also targets subsets of transposons in this early-branching land plant lineage. A comparative approach to neuroscience can greatly increase our understanding of how mechanisms map onto behaviour. A new study comparing two predatory insects demonstrates how neurons that are homologous can nonetheless mediate different computations and behaviour. Tessler et al. demonstrate that a ‘soft’ robot causes less stress to a jellyfish while handling compared to a traditional ‘hard’ robot. Evidence from live gray whale strandings suggests that their navigation may be disrupted by increased radio frequency noise generated by solar storms, suggesting the potential for magnetoreception in this species. Friess et al. discuss the results of conservation efforts for mangrove forests in recent years. DeSantis et al. respond to the concerns raised by Van Valkenburgh et al. on their original study. Van Valkenburgh et al. challenge the conclusions of a recent study by DeSantis et al. that claimed that sabertooth cats and dire wolves did not compete for similar prey. In this Primer, Moreci and Lechler follow the lifetime of an epidermal cell from its birth to its ultimate death, and detail how this journey is necessary for epidermal function. Whitewoods introduces the plant genus Utricularia. Melanins are a unique class of pigments found throughout the biosphere with a wide variety of functions, structures, and presentations. Cordero and Casadevall highlight the wide range of places melanins are found and the diverse functions they play in nature. Lissencephaly (LIS), denoting a “smooth brain,” is characterized by the absence of normal cerebral convolutions with abnormalities of cortical thickness. Androgen Receptor activity Pathogenic variants in over 20 genes are associated with LIS. The majority of posterior predominant LIS is caused by pathogenic variants in LIS1 (also known as PAFAH1B1), although a significant fraction remains without a known genetic etiology. We now implicate CEP85L as an important cause of posterior predominant LIS, identifying 13 individuals with rare, heterozygous CEP85L variants, including 2 families with autosomal dominant inheritance. We show that CEP85L is a centrosome protein localizing to the pericentriolar material, and knockdown of Cep85l causes a neuronal migration defect in mice. LIS1 also localizes to the centrosome, suggesting that this organelle is key to the mechanism of posterior predominant LIS. Genes mutated in human neuronal migration disorders encode tubulin proteins and a variety of tubulin-binding and -regulating proteins, but it is very poorly understood how these proteins function together to coordinate migration. Additionally, the way in which regional differences in neocortical migration are controlled is completely unknown. Here we describe a new syndrome with remarkably region-specific effects on neuronal migration in the posterior cortex, reflecting de novo variants in CEP85L. We show that CEP85L is required cell autonomously in vivo and in vitro for migration, that it localizes to the maternal centriole, and that it forms a complex with many other proteins required for migration, including CDK5, LIS1, NDE1, KIF2A, and DYNC1H1. Loss of CEP85L disrupts CDK5 localization and activation, leading to centrosome disorganization and disrupted microtubule cytoskeleton organization. Together, our findings suggest that CEP85L highlights a complex that controls CDK5 activity to promote neuronal migration. Under normal physiological conditions, free radical generation and antioxidant defences are balanced, and reactive oxygen species (ROS) usually act as secondary messengers in a plethora of biological processes. However, when this balance is impaired, oxidative stress develops due to imbalanced redox homeostasis resulting in cellular damage. Oxidative stress is now recognized as a trigger of cellular senescence, which is associated with multiple chronic ‘burden of lifestyle’ diseases, including atherosclerosis, type-2 diabetes, chronic kidney disease and vascular calcification; all of which possess signs of early vascular ageing. Nuclear factor erythroid 2-related factor 2 (Nrf2), termed the master regulator of antioxidant responses, is a transcription factor found to be frequently dysregulated in conditions characterized by oxidative stress and inflammation. Recent evidence suggests that activation of Nrf2 may be beneficial in protecting against vascular senescence and calcification. Both natural and synthetic Nrf2 agonists have been introduced as promising drug classes in different phases of clinical trials. However, overexpression of the Nrf2 pathway has also been linked to tumorigenesis, which highlights the requirement for further understanding of pathways involving Nrf2 activity, especially in the context of cellular senescence and vascular calcification. Therefore, comprehensive translational pre-clinical and clinical studies addressing the targeting capabilities of Nrf2 agonists are urgently required. The present review discusses the impact of Nrf2 in senescence and calcification in early vascular ageing, with focus on the potential clinical implications of Nrf2 agonists and non-pharmacological Nrf2 therapeutics. V.A 41-year-old woman was admitted with a recurrent pneumothorax coincident with menstruation 2 months after a first occurrence. Video-assisted thoracic surgery was performed for definitive diagnosis and pneumothorax treatment. Bluish diaphragmatic spots and three lung bullae were noted. A lung fistula was observed in one of the bullae, and the diaphragmatic lesion and bullae were resected. The bulla with air leakage and the diaphragmatic lesion were diagnosed as endometrial tissue via pathology. This case is rare as a fistula from a bulla with endometriosis was identified intraoperatively, suggesting the check-valve mechanism might be one of the etiologies of catamenial pneumothorax. Stent migration is a rare event with potentially serious complications including cardiac arrhythmias and heart failure. We report a case of migration of arterial stent, placed in the right iliac vein into the right pulmonary artery which was diagnosed there and subsequently not removed for at least 3 years. Despite reports in the literature for the removal of migrated stents by mini-invasive interventional methods, in our case, this was not possible, because of the long period for which the foreign body was in the right pulmonary artery and the proximal partial occlusion of organized mural thrombus.