AGO1 and AGO2 Act Redundantly in miR408-Mediated Plantacyanin Regulation

Background: In Arabidopsis, AGO1 and AGO2 associate with small RNAs that exhibit a Uridine and an Adenosine at their 59 end, respectively. Because most plant miRNAs have a 59U, AGO1 plays many essential roles in miRNA-mediated regulation of development and stress responses. In contrast, AGO2 has only been implicated in antibacterial defense in association with miR393*, which has a 59A. AGO2 also participates in antiviral defense in association with viral siRNAs. Principal Findings: This study reveals that miR408, which has a 59A, regulates its target Plantacyanin through either AGO1 or AGO2. Indeed, neither ago1 nor ago2 single mutations abolish miR408-mediated regulation of Plantacyanin. Only an ago1 ago2 double mutant appears compromised in miR408-mediated regulation of Plantacyanin, suggesting that AGO1 and AGO2 have redundant roles in this regulation. Moreover, the nature of the 59 nucleotide of miR408 does not appear essential for its regulatory role because both a wildtype 59A-MIR408 and a mutant 59U-MIR408 gene complement a mir408 mutant. Conclusions/Significance: These results suggest that miR408 associates with both AGO1 and AGO2 based on criteria that differ from the 59 end rule, reminiscent of miR390-AGO7 and miR165/166-AGO10 associations, which are not based on the nature of the 59 nucleotide

Brainstem Respiratory Oscillators Develop Independently of Neuronal Migration Defects in the Wnt/PCP Mouse Mutant looptail

The proper development and maturation of neuronal circuits require precise migration of component neurons from their birthplace (germinal zone) to their final positions. Little is known about the effects of aberrant neuronal position on the functioning of organized neuronal groups, especially in mammals. Here, we investigated the formation and properties of brainstem respiratory neurons in looptail (Lp) mutant mice in which facial motor neurons closely apposed to some respiratory neurons fail to migrate due to loss of function of the Wnt/Planar Cell Polarity (PCP) protein Vangl2. Using calcium imaging and immunostaining on embryonic hindbrain preparations, we found that respiratory neurons constituting the embryonic parafacial oscillator (e-pF) settled at the ventral surface of the medulla in Vangl2Lp/+ and Vangl2Lp/Lp embryos despite the failure of tangential migration of its normally adjacent facial motor nucleus. Anatomically, the e-pF neurons were displaced medially in Lp/+ embryos and rostro-medially Lp/Lp embryos. Pharmacological treatments showed that the e-pF oscillator exhibited characteristic network properties in both Lp/+ and Lp/Lp embryos. Furthermore, using hindbrain slices, we found that the other respiratory oscillator, the preBötzinger complex, was also anatomically and functionally established in Lp mutants. Importantly, the displaced e-pF oscillator established functional connections with the preBötC oscillator in Lp/+ mutants. Our data highlight the robustness of the developmental processes that assemble the neuronal networks mediating an essential physiological function

Transcriptional landscape of bone marrow-derived very small embryonic-like stem cells during hypoxia

<p>Abstract</p> <p>Background</p> <p>Hypoxia is a ubiquitous feature of many lung diseases and elicits cell-specific responses. While the effects of hypoxia on stem cells have been examined under <it>in vitro </it>conditions, the consequences of <it>in vivo </it>oxygen deprivation have not been studied.</p> <p>Methods</p> <p>We investigated the effects of <it>in vivo </it>hypoxia on a recently characterized population of pluripotent stem cells known as very small embryonic-like stem cells (VSELs) by whole-genome expression profiling and measuring peripheral blood stem cell chemokine levels.</p> <p>Results</p> <p>We found that exposure to hypoxia in mice mobilized VSELs from the bone marrow to peripheral blood, and induced a distinct genome-wide transcriptional signature. Applying a computationally-intensive methodology, we identified a hypoxia-induced gene interaction network that was functionally enriched in a diverse array of programs including organ-specific development, stress response, and wound repair. Topographic analysis of the network highlighted a number of densely connected hubs that may represent key controllers of stem cell response during hypoxia and, therefore, serve as putative targets for altering the pathophysiologic consequences of hypoxic burden.</p> <p>Conclusions</p> <p>A brief exposure to hypoxia recruits pluripotent stem cells to the peripheral circulation and actives diverse transcriptional programs that are orchestrated by a selective number of key genes.</p

Protection of Sinorhizobium against Host Cysteine-Rich Antimicrobial Peptides Is Critical for Symbiosis

A bacterial membrane protein, BacA, protects Sinorhizobium meliloti against the antimicrobial activity of host peptides, enabling the peptides to induce bacterial persistence rather than bacterial death

SOX2 Co-Occupies Distal Enhancer Elements with Distinct POU Factors in ESCs and NPCs to Specify Cell State

SOX2 is a master regulator of both pluripotent embryonic stem cells (ESCs) and multipotent neural progenitor cells (NPCs); however, we currently lack a detailed understanding of how SOX2 controls these distinct stem cell populations. Here we show by genome-wide analysis that, while SOX2 bound to a distinct set of gene promoters in ESCs and NPCs, the majority of regions coincided with unique distal enhancer elements, important cis-acting regulators of tissue-specific gene expression programs. Notably, SOX2 bound the same consensus DNA motif in both cell types, suggesting that additional factors contribute to target specificity. We found that, similar to its association with OCT4 (Pou5f1) in ESCs, the related POU family member BRN2 (Pou3f2) co-occupied a large set of putative distal enhancers with SOX2 in NPCs. Forced expression of BRN2 in ESCs led to functional recruitment of SOX2 to a subset of NPC-specific targets and to precocious differentiation toward a neural-like state. Further analysis of the bound sequences revealed differences in the distances of SOX and POU peaks in the two cell types and identified motifs for additional transcription factors. Together, these data suggest that SOX2 controls a larger network of genes than previously anticipated through binding of distal enhancers and that transitions in POU partner factors may control tissue-specific transcriptional programs. Our findings have important implications for understanding lineage specification and somatic cell reprogramming, where SOX2, OCT4, and BRN2 have been shown to be key factors

Effects of Climate and Atmospheric Nitrogen Deposition on Early to Mid-Term Stage Litter Decomposition Across Biomes

open263siWe acknowledge support by the German Centre for Integrative Biodiversity Research (iDiv) Halle-Jena-Leipzig, funded by the German Research Foundation (FZT 118), Scientific Grant Agency VEGA(GrantNo.2/0101/18), as well as by the European Research Council under the European Union’s Horizon 2020 Research and Innovation Program (Grant Agreement No. 677232)Litter decomposition is a key process for carbon and nutrient cycling in terrestrial ecosystems and is mainly controlled by environmental conditions, substrate quantity and quality as well as microbial community abundance and composition. In particular, the effects of climate and atmospheric nitrogen (N) deposition on litter decomposition and its temporal dynamics are of significant importance, since their effects might change over the course of the decomposition process. Within the TeaComposition initiative, we incubated Green and Rooibos teas at 524 sites across nine biomes. We assessed how macroclimate and atmospheric inorganic N deposition under current and predicted scenarios (RCP 2.6, RCP 8.5) might affect litter mass loss measured after 3 and 12 months. Our study shows that the early to mid-term mass loss at the global scale was affected predominantly by litter quality (explaining 73% and 62% of the total variance after 3 and 12 months, respectively) followed by climate and N deposition. The effects of climate were not litter-specific and became increasingly significant as decomposition progressed, with MAP explaining 2% and MAT 4% of the variation after 12 months of incubation. The effect of N deposition was litter-specific, and significant only for 12-month decomposition of Rooibos tea at the global scale. However, in the temperate biome where atmospheric N deposition rates are relatively high, the 12-month mass loss of Green and Rooibos teas decreased significantly with increasing N deposition, explaining 9.5% and 1.1% of the variance, respectively. The expected changes in macroclimate and N deposition at the global scale by the end of this century are estimated to increase the 12-month mass loss of easily decomposable litter by 1.1-3.5% and of the more stable substrates by 3.8-10.6%, relative to current mass loss. In contrast, expected changes in atmospheric N deposition will decrease the mid-term mass loss of high-quality litter by 1.4-2.2% and that of low-quality litter by 0.9-1.5% in the temperate biome. Our results suggest that projected increases in N deposition may have the capacity to dampen the climate-driven increases in litter decomposition depending on the biome and decomposition stage of substrate.openKwon T.; Shibata H.; Kepfer-Rojas S.; Schmidt I.K.; Larsen K.S.; Beier C.; Berg B.; Verheyen K.; Lamarque J.-F.; Hagedorn F.; Eisenhauer N.; Djukic I.; Caliman A.; Paquette A.; Gutierrez-Giron A.; Petraglia A.; Augustaitis A.; Saillard A.; Ruiz-Fernandez A.C.; Sousa A.I.; Lillebo A.I.; Da Rocha Gripp A.; Lamprecht A.; Bohner A.; Francez A.-J.; Malyshev A.; Andric A.; Stanisci A.; Zolles A.; Avila A.; Virkkala A.-M.; Probst A.; Ouin A.; Khuroo A.A.; Verstraeten A.; Stefanski A.; Gaxiola A.; Muys B.; Gozalo B.; Ahrends B.; Yang B.; Erschbamer B.; Rodriguez Ortiz C.E.; Christiansen C.T.; Meredieu C.; Mony C.; Nock C.; Wang C.-P.; Baum C.; Rixen C.; Delire C.; Piscart C.; Andrews C.; Rebmann C.; Branquinho C.; Jan D.; Wundram D.; Vujanovic D.; Adair E.C.; Ordonez-Regil E.; Crawford E.R.; Tropina E.F.; Hornung E.; Groner E.; Lucot E.; Gacia E.; Levesque E.; Benedito E.; Davydov E.A.; Bolzan F.P.; Maestre F.T.; Maunoury-Danger F.; Kitz F.; Hofhansl F.; Hofhansl G.; De Almeida Lobo F.; Souza F.L.; Zehetner F.; Koffi F.K.; Wohlfahrt G.; Certini G.; Pinha G.D.; Gonzlez G.; Canut G.; Pauli H.; Bahamonde H.A.; Feldhaar H.; Jger H.; Serrano H.C.; Verheyden H.; Bruelheide H.; Meesenburg H.; Jungkunst H.; Jactel H.; Kurokawa H.; Yesilonis I.; Melece I.; Van Halder I.; Quiros I.G.; Fekete I.; Ostonen I.; Borovsk J.; Roales J.; Shoqeir J.H.; Jean-Christophe Lata J.; Probst J.-L.; Vijayanathan J.; Dolezal J.; Sanchez-Cabeza J.-A.; Merlet J.; Loehr J.; Von Oppen J.; Loffler J.; Benito Alonso J.L.; Cardoso-Mohedano J.-G.; Penuelas J.; Morina J.C.; Quinde J.D.; Jimnez J.J.; Alatalo J.M.; Seeber J.; Kemppinen J.; Stadler J.; Kriiska K.; Van Den Meersche K.; Fukuzawa K.; Szlavecz K.; Juhos K.; Gerhtov K.; Lajtha K.; Jennings K.; Jennings J.; Ecology P.; Hoshizaki K.; Green K.; Steinbauer K.; Pazianoto L.; Dienstbach L.; Yahdjian L.; Williams L.J.; Brigham L.; Hanna L.; Hanna H.; Rustad L.; Morillas L.; Silva Carneiro L.; Di Martino L.; Villar L.; Fernandes Tavares L.A.; Morley M.; Winkler M.; Lebouvier M.; Tomaselli M.; Schaub M.; Glushkova M.; Torres M.G.A.; De Graaff M.-A.; Pons M.-N.; Bauters M.; Mazn M.; Frenzel M.; Wagner M.; Didion M.; Hamid M.; Lopes M.; Apple M.; Weih M.; Mojses M.; Gualmini M.; Vadeboncoeur M.; Bierbaumer M.; Danger M.; Scherer-Lorenzen M.; Ruek M.; Isabellon M.; Di Musciano M.; Carbognani M.; Zhiyanski M.; Puca M.; Barna M.; Ataka M.; Luoto M.; H. Alsafaran M.; Barsoum N.; Tokuchi N.; Korboulewsky N.; Lecomte N.; Filippova N.; Hlzel N.; Ferlian O.; Romero O.; Pinto-Jr O.; Peri P.; Dan Turtureanu P.; Haase P.; Macreadie P.; Reich P.B.; Petk P.; Choler P.; Marmonier P.; Ponette Q.; Dettogni Guariento R.; Canessa R.; Kiese R.; Hewitt R.; Weigel R.; Kanka R.; Cazzolla Gatti R.; Martins R.L.; Ogaya R.; Georges R.; Gaviln R.G.; Wittlinger S.; Puijalon S.; Suzuki S.; Martin S.; Anja S.; Gogo S.; Schueler S.; Drollinger S.; Mereu S.; Wipf S.; Trevathan-Tackett S.; Stoll S.; Lfgren S.; Trogisch S.; Seitz S.; Glatzel S.; Venn S.; Dousset S.; Mori T.; Sato T.; Hishi T.; Nakaji T.; Jean-Paul T.; Camboulive T.; Spiegelberger T.; Scholten T.; Mozdzer T.J.; Kleinebecker T.; Runk T.; Ramaswiela T.; Hiura T.; Enoki T.; Ursu T.-M.; Di Cella U.M.; Hamer U.; Klaus V.; Di Cecco V.; Rego V.; Fontana V.; Piscov V.; Bretagnolle V.; Maire V.; Farjalla V.; Pascal V.; Zhou W.; Luo W.; Parker W.; Parker P.; Kominam Y.; Kotrocz Z.; Utsumi Y.Kwon T.; Shibata H.; Kepfer-Rojas S.; Schmidt I.K.; Larsen K.S.; Beier C.; Berg B.; Verheyen K.; Lamarque J.-F.; Hagedorn F.; Eisenhauer N.; Djukic I.; Caliman A.; Paquette A.; Gutierrez-Giron A.; Petraglia A.; Augustaitis A.; Saillard A.; Ruiz-Fernandez A.C.; Sousa A.I.; Lillebo A.I.; Da Rocha Gripp A.; Lamprecht A.; Bohner A.; Francez A.-J.; Malyshev A.; Andric A.; Stanisci A.; Zolles A.; Avila A.; Virkkala A.-M.; Probst A.; Ouin A.; Khuroo A.A.; Verstraeten A.; Stefanski A.; Gaxiola A.; Muys B.; Gozalo B.; Ahrends B.; Yang B.; Erschbamer B.; Rodriguez Ortiz C.E.; Christiansen C.T.; Meredieu C.; Mony C.; Nock C.; Wang C.-P.; Baum C.; Rixen C.; Delire C.; Piscart C.; Andrews C.; Rebmann C.; Branquinho C.; Jan D.; Wundram D.; Vujanovic D.; Adair E.C.; Ordonez-Regil E.; Crawford E.R.; Tropina E.F.; Hornung E.; Groner E.; Lucot E.; Gacia E.; Levesque E.; Benedito E.; Davydov E.A.; Bolzan F.P.; Maestre F.T.; Maunoury-Danger F.; Kitz F.; Hofhansl F.; Hofhansl G.; De Almeida Lobo F.; Souza F.L.; Zehetner F.; Koffi F.K.; Wohlfahrt G.; Certini G.; Pinha G.D.; Gonzlez G.; Canut G.; Pauli H.; Bahamonde H.A.; Feldhaar H.; Jger H.; Serrano H.C.; Verheyden H.; Bruelheide H.; Meesenburg H.; Jungkunst H.; Jactel H.; Kurokawa H.; Yesilonis I.; Melece I.; Van Halder I.; Quiros I.G.; Fekete I.; Ostonen I.; Borovsk J.; Roales J.; Shoqeir J.H.; Jean-Christophe Lata J.; Probst J.-L.; Vijayanathan J.; Dolezal J.; Sanchez-Cabeza J.-A.; Merlet J.; Loehr J.; Von Oppen J.; Loffler J.; Benito Alonso J.L.; Cardoso-Mohedano J.-G.; Penuelas J.; Morina J.C.; Quinde J.D.; Jimnez J.J.; Alatalo J.M.; Seeber J.; Kemppinen J.; Stadler J.; Kriiska K.; Van Den Meersche K.; Fukuzawa K.; Szlavecz K.; Juhos K.; Gerhtov K.; Lajtha K.; Jennings K.; Jennings J.; Ecology P.; Hoshizaki K.; Green K.; Steinbauer K.; Pazianoto L.; Dienstbach L.; Yahdjian L.; Williams L.J.; Brigham L.; Hanna L.; Hanna H.; Rustad L.; Morillas L.; Silva Carneiro L.; Di Martino L.; Villar L.; Fernandes Tavares L.A.; Morley M.; Winkler M.; Lebouvier M.; Tomaselli M.; Schaub M.; Glushkova M.; Torres M.G.A.; De Graaff M.-A.; Pons M.-N.; Bauters M.; Mazn M.; Frenzel M.; Wagner M.; Didion M.; Hamid M.; Lopes M.; Apple M.; Weih M.; Mojses M.; Gualmini M.; Vadeboncoeur M.; Bierbaumer M.; Danger M.; Scherer-Lorenzen M.; Ruek M.; Isabellon M.; Di Musciano M.; Carbognani M.; Zhiyanski M.; Puca M.; Barna M.; Ataka M.; Luoto M.; H. Alsafaran M.; Barsoum N.; Tokuchi N.; Korboulewsky N.; Lecomte N.; Filippova N.; Hlzel N.; Ferlian O.; Romero O.; Pinto-Jr O.; Peri P.; Dan Turtureanu P.; Haase P.; Macreadie P.; Reich P.B.; Petk P.; Choler P.; Marmonier P.; Ponette Q.; Dettogni Guariento R.; Canessa R.; Kiese R.; Hewitt R.; Weigel R.; Kanka R.; Cazzolla Gatti R.; Martins R.L.; Ogaya R.; Georges R.; Gaviln R.G.; Wittlinger S.; Puijalon S.; Suzuki S.; Martin S.; Anja S.; Gogo S.; Schueler S.; Drollinger S.; Mereu S.; Wipf S.; Trevathan-Tackett S.; Stoll S.; Lfgren S.; Trogisch S.; Seitz S.; Glatzel S.; Venn S.; Dousset S.; Mori T.; Sato T.; Hishi T.; Nakaji T.; Jean-Paul T.; Camboulive T.; Spiegelberger T.; Scholten T.; Mozdzer T.J.; Kleinebecker T.; Runk T.; Ramaswiela T.; Hiura T.; Enoki T.; Ursu T.-M.; Di Cella U.M.; Hamer U.; Klaus V.; Di Cecco V.; Rego V.; Fontana V.; Piscov V.; Bretagnolle V.; Maire V.; Farjalla V.; Pascal V.; Zhou W.; Luo W.; Parker W.; Parker P.; Kominam Y.; Kotrocz Z.; Utsumi Y

Creation of forest edges has a global impact on forest vertebrates

Forest edges influence more than half of the world's forests and contribute to worldwide declines in biodiversity and ecosystem functions. However, predicting these declines is challenging in heterogeneous fragmented landscapes. Here we assembled a global dataset on species responses to fragmentation and developed a statistical approach for quantifying edge impacts in heterogeneous landscapes to quantify edge-determined changes in abundance of 1,673 vertebrate species. We show that the abundances of 85% of species are affected, either positively or negatively, by forest edges. Species that live in the centre of the forest (forest core), that were more likely to be listed as threatened by the International Union for Conservation of Nature (IUCN), reached peak abundances only at sites farther than 200-400 m from sharp high-contrast forest edges. Smaller-bodied amphibians, larger reptiles and medium-sized non-volant mammals experienced a larger reduction in suitable habitat than other forest-core species. Our results highlight the pervasive ability of forest edges to restructure ecological communities on a global scale

Effects of climate and atmospheric nitrogen deposition on early to mid-term stage litter decomposition across biomes

Litter decomposition is a key process for carbon and nutrient cycling in terrestrial ecosystems and is mainly controlled by environmental conditions, substrate quantity and quality as well as microbial community abundance and composition. In particular, the effects of climate and atmospheric nitrogen (N) deposition on litter decomposition and its temporal dynamics are of significant importance, since their effects might change over the course of the decomposition process. Within the TeaComposition initiative, we incubated Green and Rooibos teas at 524 sites across nine biomes. We assessed how macroclimate and atmospheric inorganic N deposition under current and predicted scenarios (RCP 2.6, RCP 8.5) might affect litter mass loss measured after 3 and 12 months. Our study shows that the early to mid-term mass loss at the global scale was affected predominantly by litter quality (explaining 73% and 62% of the total variance after 3 and 12 months, respectively) followed by climate and N deposition. The effects of climate were not litter-specific and became increasingly significant as decomposition progressed, with MAP explaining 2% and MAT 4% of the variation after 12 months of incubation. The effect of N deposition was litter-specific, and significant only for 12-month decomposition of Rooibos tea at the global scale. However, in the temperate biome where atmospheric N deposition rates are relatively high, the 12-month mass loss of Green and Rooibos teas decreased significantly with increasing N deposition, explaining 9.5% and 1.1% of the variance, respectively. The expected changes in macroclimate and N deposition at the global scale by the end of this century are estimated to increase the 12-month mass loss of easily decomposable litter by 1.1-3.5% and of the more stable substrates by 3.8-10.6%, relative to current mass loss. In contrast, expected changes in atmospheric N deposition will decrease the mid-term mass loss of high-quality litter by 1.4-2.2% and that of low-quality litter by 0.9-1.5% in the temperate biome. Our results suggest that projected increases in N deposition may have the capacity to dampen the climate-driven increases in litter decomposition depending on the biome and decomposition stage of substrate. © Copyright © 2021 Kwon, Shibata, Kepfer-Rojas, Schmidt, Larsen, Beier, Berg, Verheyen, Lamarque, Hagedorn, Eisenhauer, Djukic and TeaComposition Network