Phenotypic plasticity in sargassum forests may not counteract projected biomass losses along a broad latitudinal gradient

Phenotypic plasticity and local adaptation can adjust individual responses to environmental changes across species' ranges. Studies addressing the implications of such traits have been underrepresented in the marine environment. Sargassum cymosum represents an ideal model to test phenotypic plasticity, as populations along the southwestern Atlantic Ocean display a sharp decrease in abundance toward distributional range limits. We (1) characterized the macroecological environment of S. cymosum across a latitudinal gradient, (2) evaluated potential differences in ecophysiological adjustments (biomass, photosynthetic pigments, phenolic compounds, total soluble sugars and proteins, and carbon-nitrogen-CN-content), and (3) tested for differences in thermal tolerance based on time series analyses produced from the present to contrasting representative concentration pathways scenarios (RCP) of future climate changes. Our results showed distinct macroecological environments, corresponding to tropical and warm temperate conditions, driving biomass and ecophysiological adjustments of S. cymosum. Populations from the two environments displayed contrasting thermal tolerances, with tropical individuals better coping with thermal stress when compared to more temperate ones (lethal temperatures of 33 degrees C vs. 30 degrees C); yet both populations lose biomass in response to increasing thermal stress while increasing secondary metabolites (for example, carotenoids and phenolic compounds) and decrease chlorophyll's content, Fv/Fm, total soluble sugars concentration and CN ratio, owing to oxidative stress. Despite evidence for phenotypic plasticity, significant future losses might occur in both tropical and warm temperate populations, particularly under the no mitigation RCP scenario, also known as the business as usual (that is, 8.5). In this context, broad compliance with the Paris Agreement might counteract projected impacts of climate change, safeguarding Sargassum forests in the years to come.This study was supported by grants from Boticario Foundation, FAPESC-Foundation Support Research and Innovation in the State of Santa Catarina, Capes Higher Education Personnel Improvement Coordination, CNPq-National Council for Scientific and Technological Development, Petrobras Ambiental, REBENTOS-Habitat monitoring network coastal Benthic and ProspecMar-Islands Sustainable Prospecting in Ocean Islands: Biodiversity, Chemistry, Ecology and Biotechnology, Rede Coral Vivo, REDEALGAS, a Pew Marine Fellowship, the Foundation for Science and Technology (FCT) of Portugal via SFRH/BSAB/150485/2019, SFRH/BD/144878/2019, UID/Multi/04326/2019, PTDC/BIA-CBI/6515/2020 and the transitional norm DL57/2016/CP1361/CT0035. LPG received a doctorate scholarship (88882.438723/2019-01) from Capes. CFDG thanks CNPq grants PQ-309658/2016-0and306304/2019-8. PAH thanks CAPES-Senior Visitor, CAPESPrInt 310793/2018-01, CNPq-PVE 407365/2013-3, CNPq-Universal 426215/2016-8 and CNPq-PQ308537/2019-0. GK received a master's scholarship from CAPES.info:eu-repo/semantics/submittedVersio

Histamine H-3 Receptors Decrease Dopamine Release in the Ventral Striatum by Reducing the Activity of Striatal Cholinergic Interneurons

Histamine H-3 receptors are widely distributed Gi-coupled receptors whose activation reduces neuronal activity and inhibits release of numerous neurotransmitters. Although these receptors are abundantly expressed in the striatum, their modulatory role on activity-dependent dopamine release is not well understood. Here, we observed that histamine H-3 receptor activation indirectly diminishes dopamine overflow in the ventral striatum by reducing cholinergic interneuron activity. Acute brain slices from C57BL/6 or channelrhodopsin-2-transfected DAT-cre mice were obtained, and dopamine transients evoked either electrically or optogenetically were measured by fast-scan cyclic voltammetry. The H-3 agonist alpha-methylhistamine significantly reduced electrically-evoked dopamine overflow, an effect blocked by the nicotinic acetylcholine receptor antagonist dihydro-beta-erythroidine, suggesting involvement of cholinergic interneurons. None of the drug treatments targeting H-3 receptors affected optogenetically evoked dopamine overflow, indicating that direct H-3-modulation of dopaminergic axons is unlikely. Next, we used qPCR and confirmed the expression of histamine H-3 receptor mRNA in cholinergic interneurons, both in ventral and dorsal striatum. Activation of H-3 receptors by alpha-methylhistamine reduced spontaneous firing of cholinergic interneurons in the ventral, but not in the dorsal striatum. Resting membrane potential and number of spontaneous action potentials in ventral-striatal cholinergic interneurons were significantly reduced by alpha-methylhistamine. Acetylcholine release from isolated striatal synaptosomes, however, was not altered by alpha-methylhistamine. Together, these results indicate that histamine H-3 receptors are important modulators of dopamine release, specifically in the ventral striatum, and that they do so by decreasing the firing rate of cholinergic neurons and, consequently, reducing cholinergic tone on dopaminergic axons. (C) 2018 IBRO. Published by Elsevier Ltd. All rights reserved.Peer reviewe

Empirical Evidence for Son-Killing X Chromosomes and the Operation of SA-Zygotic Drive

Diploid organisms have two copies of all genes, but only one is carried by each haploid gamete and diploid offspring. This causes a fundamental genetic conflict over transmission rate between alternative alleles. Single genes, or gene clusters, only rarely code for the complex phenotypes needed to give them a transmission advantage (drive phenotype). However, all genes on a male's X and Y chromosomes co-segregate, allowing different sex-linked genes to code for different parts of the drive phenotype. Correspondingly, the well-characterized phenomenon of male gametic drive, occurring during haploid gametogenesis, is especially common on sex chromosomes. The new theory of sexually antagonistic zygotic drive of the sex chromosomes (SA-zygotic drive) extends the logic of gametic drive into the diploid phase of the lifecycle, whenever there is competition among siblings or harmful sib-sib mating. The X and Y are predicted to gain a transmission advantage by harming offspring of the sex that does not carry them.Here we analyzed a mutant X-chromosome in Drosophila simulans that produced an excess of daughters when transmitted from males. We developed a series of tests to differentiate between gametic and SA-zygotic drive, and provide multiple lines of evidence that SA-zygotic drive is responsible for the sex ratio bias. Driving sires produce about 50% more surviving daughters than sons.Sex-ratio distortion due to genetic conflict has evolved via gametic drive and maternally transmitted endosymbionts. Our data indicate that sex chromosomes can also drive by harming the non-carrier sex of offspring

Genome of Rhodnius prolixus, an insect vector of Chagas disease, reveals unique adaptations to hematophagy and parasite infection

Rhodnius prolixus not only has served as a model organism for the study of insect physiology, but also is a major vector of Chagas disease, an illness that affects approximately seven million people worldwide. We sequenced the genome of R. prolixus, generated assembled sequences covering 95% of the genome ( approximately 702 Mb), including 15,456 putative protein-coding genes, and completed comprehensive genomic analyses of this obligate blood-feeding insect. Although immune-deficiency (IMD)-mediated immune responses were observed, R. prolixus putatively lacks key components of the IMD pathway, suggesting a reorganization of the canonical immune signaling network. Although both Toll and IMD effectors controlled intestinal microbiota, neither affected Trypanosoma cruzi, the causal agent of Chagas disease, implying the existence of evasion or tolerance mechanisms. R. prolixus has experienced an extensive loss of selenoprotein genes, with its repertoire reduced to only two proteins, one of which is a selenocysteine-based glutathione peroxidase, the first found in insects. The genome contained actively transcribed, horizontally transferred genes from Wolbachia sp., which showed evidence of codon use evolution toward the insect use pattern. Comparative protein analyses revealed many lineage-specific expansions and putative gene absences in R. prolixus, including tandem expansions of genes related to chemoreception, feeding, and digestion that possibly contributed to the evolution of a blood-feeding lifestyle. The genome assembly and these associated analyses provide critical information on the physiology and evolution of this important vector species and should be instrumental for the development of innovative disease control methods

How to make a sex chromosome

Sex chromosomes can evolve once recombination is halted between a homologous pair of chromosomes. Owing to detailed studies using key model systems, we have a nuanced understanding and a rich review literature of what happens to sex chromosomes once recombination is arrested. However, three broad questions remain unanswered. First, why do sex chromosomes stop recombining in the first place? Second, how is recombination halted? Finally, why does the spread of recombination suppression, and therefore the rate of sex chromosome divergence, vary so substantially across clades? In this review, we consider each of these three questions in turn to address fundamental questions in the field, summarize our current understanding, and highlight important areas for future work