scholarly journals Studying the genetic basis of masting

2021 ◽  
Vol 376 (1839) ◽  
Author(s):  
Akiko Satake ◽  
Dave Kelly
Keyword(s):  
Genetic Basis ◽  
Molecular Mechanisms ◽  
Mast Seeding ◽  
Ecological Genomics ◽  
Theme Issue ◽  
Natural Conditions ◽  
Genetic Level ◽  
Seed Crops

The mechanisms underlying mast seeding have traditionally been studied by collecting long-term observational data on seed crops and correlating seedfall with environmental variables. Significant progress in ecological genomics will improve our understanding of the evolution of masting by clarifying the genetic basis of masting traits and the role of natural selection in shaping those traits. Here, we summarize three important aspects in studying the evolution of masting at the genetic level: which traits govern masting, whether those traits are genetically regulated, and which taxa show wide variation in these traits. We then introduce recent studies on the molecular mechanisms of masting. Those studies measure seasonal changes in gene expression in natural conditions to quantify how multiple environmental factors combine to regulate floral initiation, which in many masting plant species is the single largest contributor to among-year variation in seed crops. We show that Fagaceae offers exceptional opportunities for evolutionary investigations because of its diversity at both the phenotypic and genetic levels and existing documented genome sequences. This article is part of the theme issue ‘The ecology and evolution of synchronized seed production in plants’.

Potential Role of Adult Hippocampal Neurogenesis in Traumatic Brain Injury

2021 ◽  
Vol 28 ◽  
Author(s):  
Lucas Alexandre Santos Marzano ◽  
Fabyolla Lúcia Macedo de Castro ◽  
Caroline Amaral Machado ◽  
João Luís Vieira Monteiro de Barros ◽  
Thiago Macedo e Cordeiro ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Clinical Studies ◽  
Molecular Mechanisms ◽  
Hippocampal Neurogenesis ◽  
Cognitive Outcomes ◽  
Adult Hippocampal Neurogenesis ◽  
The Brain

: Traumatic brain injury (TBI) is a serious cause of disability and death among young and adult individuals, displaying complex pathophysiology including cellular and molecular mechanisms that are not fully elucidated. Many experimental and clinical studies investigated the potential relationship between TBI and the process by which neurons are formed in the brain, known as neurogenesis. Currently, there are no available treatments for TBI’s long-term consequences being the search for novel therapeutic targets, a goal of highest scientific and clinical priority. Some studies evaluated the benefits of treatments aimed at improving neurogenesis in TBI. In this scenario, herein, we reviewed current pre-clinical studies that evaluated different approaches to improving neurogenesis after TBI while achieving better cognitive outcomes, which may consist in interesting approaches for future treatments.

scholarly journals Neuroinflammation and Its Impact on the Pathogenesis of COVID-19

2021 ◽  
Vol 8 ◽  
Author(s):  
Mohammed M. Almutairi ◽  
Farzane Sivandzade ◽  
Thamer H. Albekairi ◽  
Faleh Alqahtani ◽  
Luca Cucullo
Keyword(s):  
Immune System ◽  
Molecular Mechanisms ◽  
Potential Role ◽  
Immune Cell ◽  
Clinical Manifestations ◽  
Cell Infiltration ◽  
Cellular Mechanisms ◽  
Cytokine Levels

Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The clinical manifestations of COVID-19 include dry cough, difficult breathing, fever, fatigue, and may lead to pneumonia and respiratory failure. There are significant gaps in the current understanding of whether SARS-CoV-2 attacks the CNS directly or through activation of the peripheral immune system and immune cell infiltration. Although the modality of neurological impairments associated with COVID-19 has not been thoroughly investigated, the latest studies have observed that SARS-CoV-2 induces neuroinflammation and may have severe long-term consequences. Here we review the literature on possible cellular and molecular mechanisms of SARS-CoV-2 induced-neuroinflammation. Activation of the innate immune system is associated with increased cytokine levels, chemokines, and free radicals in the SARS-CoV-2-induced pathogenic response at the blood-brain barrier (BBB). BBB disruption allows immune/inflammatory cell infiltration into the CNS activating immune resident cells (such as microglia and astrocytes). This review highlights the molecular and cellular mechanisms involved in COVID-19-induced neuroinflammation, which may lead to neuronal death. A better understanding of these mechanisms will help gain substantial knowledge about the potential role of SARS-CoV-2 in neurological changes and plan possible therapeutic intervention strategies.

scholarly journals Molecular Mechanisms of Oxytocin Signaling at the Synaptic Connection

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Jan Bakos ◽  
Annamaria Srancikova ◽  
Tomas Havranek ◽  
Zuzana Bacova
Keyword(s):  
Neurodevelopmental Disorders ◽  
Molecular Mechanisms ◽  
Neuronal Excitability ◽  
Molecular Level ◽  
Short Term ◽  
Oxytocin Receptors ◽  
Potential Therapeutic Intervention ◽  
Early Alteration

Aberrant regulation of oxytocin signaling is associated with the etiology of neurodevelopmental disorders. Synaptic dysfunctions in neurodevelopmental disorders are becoming increasingly known, and their pathogenic mechanisms could be a target of potential therapeutic intervention. Therefore, it is important to pay attention to the role of oxytocin and its receptor in synapse structure, function, and neuron connectivity. An early alteration in oxytocin signaling may disturb neuronal maturation and may have short-term and long-term pathological consequences. At the molecular level, neurodevelopmental disorders include alterations in cytoskeletal rearrangement and neuritogenesis resulting in a diversity of synaptopathies. The presence of oxytocin receptors in the presynaptic and postsynaptic membranes and the direct effects of oxytocin on neuronal excitability by regulating the activity of ion channels in the cell membrane implicate that alterations in oxytocin signaling could be involved in synaptopathies. The ability of oxytocin to modulate neurogenesis, synaptic plasticity, and certain parameters of cytoskeletal arrangement is discussed in the present review.

scholarly journals Role of LAMP1 Binding and pH Sensing by the Spike Complex of Lassa Virus

2016 ◽  
Vol 90 (22) ◽  
pp. 10329-10338 ◽  
Author(s):  
Hadas Cohen-Dvashi ◽  
Hadar Israeli ◽  
Orly Shani ◽  
Aliza Katz ◽  
Ron Diskin
Keyword(s):  
Membrane Fusion ◽  
Molecular Mechanisms ◽  
Cell Entry ◽  
Lassa Virus ◽  
Dependent Manner ◽  
Acidic Ph ◽  
Ph Sensing ◽  
Positively Charged

ABSTRACTTo effectively infect cells, Lassa virus needs to switch in an endosomal compartment from its primary receptor, α-dystroglycan, to a protein termed LAMP1. A unique histidine triad on the surface of the receptor-binding domain from the glycoprotein spike complex of Lassa virus is important for LAMP1 binding. Here we investigate mutated spikes that have an impaired ability to interact with LAMP1 and show that although LAMP1 is important for efficient infectivity, it is not required for spike-mediated membrane fusionper se. Our studies reveal important regulatory roles for histidines from the triad in sensing acidic pH and preventing premature spike triggering. We further show that LAMP1 requires a positively charged His230 residue to engage with the spike complex and that LAMP1 binding promotes membrane fusion. These results elucidate the molecular role of LAMP1 binding during Lassa virus cell entry and provide new insights into how pH is sensed by the spike.IMPORTANCELassa virus is a devastating disease-causing agent in West Africa, with a significant yearly death toll and severe long-term complications associated with its infection in survivors. In recent years, we learned that Lassa virus needs to switch receptors in a pH-dependent manner to efficiently infect cells, but neither the molecular mechanisms that allow switching nor the actual effects of switching were known. Here we investigate the activity of the viral spike complex after abrogation of its ability to switch receptors. These studies inform us about the role of switching receptors and provide new insights into how the spike senses acidic pH.

Therapeutic Advances in Myeloproliferative Neoplasms: The Role of New-Small Molecule Inhibitors

2012 ◽  
pp. 406-410 ◽  
Author(s):  
Srdan Verstovsek
Keyword(s):  
Molecular Mechanisms ◽  
Therapeutic Potential ◽  
Myeloproliferative Neoplasms ◽  
Janus Kinase ◽  
Treatment Focus ◽  
Rational Combination ◽  
Short And Long Term ◽  
Jak2 Inhibitors

Overview: The discovery that a somatic point mutation (JAK2V617F) in the Janus kinase 2 ( JAK2) is highly prevalent in patients with myeloproliferative neoplasms (MPNs) has been a crucial breakthrough in our understanding of the underlying molecular mechanisms of these diseases. Therefore, preclinical and clinical research in recent years has focused intensely on the development of new therapies targeted to JAK2. These efforts culminated in recent approval of ruxolitinib as the first official therapy for patients with intermediate- or high-risk myelofibrosis (MF). Therapy with JAK2 inhibitors substantially improves quality of life and reduces organomegaly in MF with or without JAKV617F mutation. Recent results suggest that patients with advanced MF may live longer when receiving therapy with ruxolitinib. However, JAK2 inhibitors do not eliminate the disease and new medications are needed to expand on the benefits seen with JAK2 inhibitors. Although many agents are still in the early stages of development, the wealth of publications and presentations has continued to support our growing understanding of the pathophysiology of MF as well as the potential short- and long-term outcomes of these new and diverse approaches to treatment. Focus of ongoing efforts is particularly on the improvements in anemia and fibrosis, as well as on rational combination trials of JAK2 inhibitors and other potentially active agents. Therapeutic potential and limitations of JAK2 inhibitors and other novel medications in clinical studies are reviewed.

scholarly journals Genomics of long- and short- term adaptation in maize and teosinte

2018 ◽  
Author(s):  
Anne Lorant ◽  
Jeffrey Ross-Ibarra ◽  
Maud Tenaillon
Keyword(s):  
Natural Variation ◽  
Genetic Basis ◽  
Wild Relatives ◽  
Short Term ◽  
Short Term Adaptation ◽  
Maize Domestication ◽  
Cultivated Populations ◽  
Genetic Bases

Maize is an excellent model for the study of plant adaptation. Indeed, post domestication maize quickly adapted to a host of new environments across the globe. And work over the last decade has begun to highlight the role of the wild relatives of maize – the teosintes Zea mays ssp. parviglumis and ssp. mexicana – as excellent models for dissecting long-term local adaptation. Although human-driven selection associated with maize domestication has been extensively studied, the genetic bases of natural variation is still poorly understood. Here we review studies on the genetic basis of adaptation and plasticity in maize and its wild relatives. We highlight a range of different processes that contribute to adaptation and discuss evidence from natural, cultivated, and experimental populations. From an applied perspective, understanding the genetic bases of adaptation and the contribution of plasticity will provide us with new tools to both better understand and mitigate the effect of climate changes on natural and cultivated populations.

scholarly journals An exon DNA element modulates heterochromatin spreading in the master regulator for sexual commitment in malaria parasites

2020 ◽  
Author(s):  
Carlos Cordon-Obras ◽  
Anna Barcons-Simon ◽  
Christine Scheidig-Benatar ◽  
Aurelie Claës ◽  
Valentin Sabatet ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Rna Binding ◽  
Antigenic Variation ◽  
Rna Binding Proteins ◽  
Protein Complexes ◽  
Heterochromatin Protein 1 ◽  
Master Regulator ◽  
Heterochromatin Protein

ABSTRACTHeterochromatin is essential in all eukaryotes to maintain genome integrity, long-term gene repression and to help chromosome segregation during mitosis. However, heterochromatin regions must be restricted by boundary elements to avoid its spreading over actively transcribed loci. In Plasmodium falciparum, facultative heterochromatin is important to regulate parasite virulence, antigenic variation and transmission. However, the underlying molecular mechanisms regulating repressive regions remain unknown. To investigate this topic, we chose the ap2-g gene, which forms a strictly delimited and independent heterochromatin island. Using electrophoretic motility shift assay (EMSA) we identified an ap2-g exon element at the 3’ end binding nuclear protein complexes. Upon replacement of this region by a gfp gene, we observed a shift in the heterochromatin boundary resulting in HP1 (Heterochromatin Protein 1) spreading over ∼2 additional kb downstream. We used this DNA element to purify candidate proteins followed by proteomic analysis. The identified complexes were found to be enriched in RNA-binding proteins, pointing to a potential role of RNA in the regulation of the ap2-g 3’ heterochromatin boundary. Our results provide insight into the unexplored topic of heterochromatin biology in P. falciparum and identify a DNA element within the master regulator of sexual commitment modulating heterochromatin spreading.

Molecular mechanisms of synaptic consolidation during sleep: BDNF function and dendritic protein synthesis

2005 ◽  
Vol 28 (1) ◽  
pp. 65-66
Author(s):  
Clive R. Bramham
Keyword(s):  
Memory Consolidation ◽  
Molecular Mechanisms ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Dendritic Protein Synthesis ◽  
Mechanisms Of Memory ◽  
Activity Dependent ◽  
Specific Contribution

Insights into the role of sleep in the molecular mechanisms of memory consolidation may come from studies of activity-dependent synaptic plasticity, such as long-term potentiation (LTP). This commentary posits a specific contribution of sleep to LTP stabilization, in which mRNA transported to dendrites during wakefulness is translated during sleep. Brain-derived neurotrophic factor may drive the translation of newly transported and resident mRNA.

scholarly journals Nutrients and Oxidative Stress: Friend or Foe?

2018 ◽  
Vol 2018 ◽  
pp. 1-24 ◽  
Author(s):  
Bee Ling Tan ◽  
Mohd Esa Norhaizan ◽  
Winnie-Pui-Pui Liew
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanisms ◽  
Noncommunicable Diseases ◽  
Intrinsic Factors ◽  
Fat Consumption ◽  
Dietary Choices ◽  
Protein Diets ◽  
Cell Signaling Pathways

There are different types of nutritionally mediated oxidative stress sources that trigger inflammation. Much information indicates that high intakes of macronutrients can promote oxidative stress and subsequently contribute to inflammation via nuclear factor-kappa B- (NF-κB-) mediated cell signaling pathways. Dietary carbohydrates, animal-based proteins, and fats are important to highlight here because they may contribute to the long-term consequences of nutritionally mediated inflammation. Oxidative stress is a central player of metabolic ailments associated with high-carbohydrate and animal-based protein diets and excessive fat consumption. Obesity has become an epidemic and represents the major risk factor for several chronic diseases, including diabetes, cardiovascular disease (CVD), and cancer. However, the molecular mechanisms of nutritionally mediated oxidative stress are complex and poorly understood. Therefore, this review aimed to explore how dietary choices exacerbate or dampen the oxidative stress and inflammation. We also discussed the implications of oxidative stress in the adipocyte and glucose metabolism and obesity-associated noncommunicable diseases (NCDs). Taken together, a better understanding of the role of oxidative stress in obesity and the development of obesity-related NCDs would provide a useful approach. This is because oxidative stress can be mediated by both extrinsic and intrinsic factors, hence providing a plausible means for the prevention of metabolic disorders.

scholarly journals Longevity: epigenetic and biomolecular aspects

2015 ◽  
Vol 6 (2) ◽  
pp. 105-117 ◽  
Author(s):  
Giusi Taormina ◽  
Mario G. Mirisola
Keyword(s):  
Simple Model ◽  
Molecular Mechanisms ◽  
Model Organisms ◽  
Intermittent Fasting ◽  
Epigenetic Mechanisms ◽  
Long Term Effects ◽  
Dietary Interventions ◽  
Aging Theories

AbstractMany aging theories and their related molecular mechanisms have been proposed. Simple model organisms such as yeasts, worms, fruit flies and others have massively contributed to their clarification, and many genes and pathways have been associated with longevity regulation. Among them, insulin/IGF-1 plays a key and evolutionary conserved role. Interestingly, dietary interventions can modulate this pathway. Calorie restriction (CR), intermittent fasting, and protein and amino acid restriction prolong the lifespan of mammals by IGF-1 regulation. However, some recent findings support the hypothesis that the long-term effects of diet also involve epigenetic mechanisms. In this review, we describe the best characterized aging pathways and highlight the role of epigenetics in diet-mediated longevity.

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