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Abstract Plant disease resistance is a complex process that is maintained in an intricate balance with development. Increasing evidence indicates the importance of posttranscriptional regulation of plant defense by RNA binding proteins. In a genetic screen for suppressors of Arabidopsis (Arabidopsis thaliana) accelerated cell death 6-1 (acd6-1), a small constitutive defense mutant whose defense level is grossly in a reverse proportion to plant size, we identified an allele of the canonical flowering regulatory gene FLOWERING LOCUS K HOMOLOGY DOMAIN (FLK) encoding a putative protein with triple K homology (KH) repeats. The KH repeat is an ancient RNA binding motif found in proteins from diverse organisms. The relevance of KH-domain proteins in pathogen resistance is largely unexplored. In addition to late flowering, the flk mutants exhibited decreased resistance to the bacterial pathogen Pseudomonas syringae and increased resistance to the necrotrophic fungal pathogen Botrytis cinerea. We further found that the flk mutations compromised basal defense and defense signaling mediated by salicylic acid (SA). Mutant analysis revealed complex genetic interactions between FLK and several major SA pathway genes. RNA-seq data showed that FLK regulates expression abundance of some major defense- and development-related genes as well as alternative splicing of a number of genes. Among the genes affected by FLK is ACD6, whose transcripts had increased intron retentions influenced by the flk mutations. Thus, this study provides mechanistic support for flk suppression of acd6-1 and establishes that FLK is a multifunctional gene involved in regulating pathogen defense and development of plants. 

Recent studies have demonstrated the importance of temporal regulation of pathogen defense by the circadian clock. However, our understanding of the molecular basis underlying this role of the circadian clock is still in its infancy. We report here the mechanism by which the Arabidopsis master clock protein CCA1 regulates an output target gene GRP7 for its circadian expression and function in pathogen defense. Our data firmly establish that CCA1 physically associates with the GRP7 promoter via the predicted CCA1-binding motif, evening element (EE). A site-directed mutagenesis study showed that while individual EE motifs differentially contribute to robust circadian expression of GRP7, abolishing all four EE motifs in the proximal GRP7 promoter disrupts rhythmicity of GRP7 expression and results in misalignment of defense signaling mediated by GRP7 and altered pathogen responses. This study provides a mechanistic link of the circadian regulation of an output gene to its biological function in pathogen defense, underscoring the importance of temporal control of plant innate immunity.

 

Abstract. This study quantifies differences among four widely usedatmospheric reanalysis datasets (ERA5, JRA-55, MERRA-2, and CFSR) in theirrepresentation of the dynamical changes induced by springtime polarstratospheric ozone depletion in the Southern Hemisphere from 1980 to 2001.The intercomparison is undertaken as part of the SPARC(Stratosphere–troposphere Processes and their Role in Climate) ReanalysisIntercomparison Project (S-RIP). The reanalyses are generally in goodagreement in their representation of the strengthening of the lowerstratospheric polar vortex during the austral spring–summer season,associated with reduced radiative heating due to ozone loss, as well as thedescent of anomalously strong westerly winds into the troposphere duringsummer and the subsequent poleward displacement and intensification of thepolar front jet. Differences in the trends in zonal wind between thereanalyses are generally small compared to the mean trends. The exception isCFSR, which exhibits greater disagreement compared to the other threereanalysis datasets, with stronger westerly winds in the lower stratospherein spring and a larger poleward displacement of the tropospheric westerlyjet in summer. The dynamical changes associated with the ozone hole are examined byinvestigating the momentum budget and then the eddy heat and momentumfluxes in terms of planetary- and synoptic-scale Rossby wave contributions.The dynamical changes are consistently represented across the reanalysesand support our dynamical understanding of the response of the coupledstratosphere–troposphere system to the ozone hole. Although our resultssuggest a high degree of consistency across the four reanalysis datasets inthe representation of these dynamical changes, there are larger differencesin the wave forcing, residual circulation, and eddy propagation changes compared to the zonal wind trends. In particular, there is a noticeabledisparity in these trends in CFSR compared to the other three reanalyses,while the best agreement is found between ERA5 and JRA-55. Greateruncertainty in the components of the momentum budget, as opposed to meancirculation, suggests that the zonal wind is better constrained by theassimilation of observations compared to the wave forcing, residualcirculation, and eddy momentum and heat fluxes, which are more dependent onthe model-based forecasts that can differ between reanalyses. Lookingforward, however, these findings give us confidence that reanalysis datasetscan be used to assess changes associated with the ongoing recovery ofstratospheric ozone. 

High surface temperatures are important in Antarctica because of their role in ice melt and sea level rise. We investigate a high temperature event in December 1989 that gave record temperatures in coastal East Antarctica between 60° and 100°E. The high temperatures were associated with a pool of warm lower tropospheric air with December temperature anomalies of >14°C that developed in two stages over the Amery Ice Shelf. First, there was near‐record poleward warm advection within an atmospheric river. Second, synoptically driven downslope flow from the interior reached unprecedented December strength over a large area, leading to strong descent and further warming in the coastal region. The coastal easterly winds were unusually deep and strong, and the warm pool was advected westwards, giving a short period of high temperatures at coastal locations, including a surface temperature of 9.3°C at Mawson, the second highest in its 66‐year record.

 

ABSTRACT During their parasitic life cycle, through sandflies and vertebrate hosts, Leishmania parasites confront strikingly different environments, including abrupt changes in pH and temperature, to which they must rapidly adapt. These adaptations include alterations in Leishmania gene expression, metabolism, and morphology, allowing them to thrive as promastigotes in the sandfly and as intracellular amastigotes in the vertebrate host. A critical aspect of Leishmania metabolic adaptation to these changes is maintenance of efficient mitochondrial function in the hostile vertebrate environment. Such functions, including generation of ATP, depend upon the expression of many mitochondrial proteins, including subunits of cytochrome c oxidase (COX). Significantly, under mammalian temperature conditions, expression of Leishmania major COX subunit IV (LmCOX4) and virulence are dependent upon two copies of LACK , a gene that encodes the ribosome-associated scaffold protein, LACK ( Leishmania ortholog of RACK1 [receptor for activated C kinase]). Targeted replacement of an endogenous LACK copy with a putative ribosome-binding motif-disrupted variant (LACK R34D35G36 →LACK D34D35E36 ) resulted in thermosensitive parasites that showed diminished LmCOX4 expression, mitochondrial fitness, and replication in macrophages. Surprisingly, despite these phenotypes, LACK D34D35E36 associated with monosomes and polysomes and showed no major impairment of global protein synthesis. Collectively, these data suggest that wild-type (WT) LACK orchestrates robust LmCOX4 expression and mitochondrial fitness to ensure parasite virulence, via optimized functional interactions with the ribosome. IMPORTANCE Leishmania parasites are trypanosomatid protozoans that persist in infected human hosts to cause a spectrum of pathologies, from cutaneous and mucocutaneous manifestations to visceral leishmaniasis caused by Leishmania donovani . The latter is usually fatal if not treated. Persistence of L. major in the mammalian host depends upon maintaining gene-regulatory programs to support essential parasite metabolic functions. These include expression and assembly of mitochondrial L. major cytochrome c oxidase (LmCOX) subunits, important for Leishmania ATP production. Significantly, under mammalian conditions, WT levels of LmCOX subunits require threshold levels of the Leishmania ribosome-associated scaffold protein, LACK. Unexpectedly, we find that although disruption of LACK’s putative ribosome-binding motif does not grossly perturb ribosome association or global protein synthesis, it nonetheless impairs COX subunit expression, mitochondrial function, and virulence. Our data indicate that the quality of LACK’s interaction with Leishmania ribosomes is critical for LmCOX subunit expression and parasite mitochondrial function in the mammalian host. Collectively, these findings validate LACK’s ribosomal interactions as a potential therapeutic target. 

The boreal‐winter stratospheric polar vortex is more disturbed when the quasi‐biennial oscillation (QBO) in the lower stratosphere is in its easterly phase (eQBO), and more stable during the westerly phase (wQBO). This so‐called “Holton–Tan effect” (HTE) is known to involve Rossby waves (RWs) but the details remain obscure. This tropical–extratropical connection is re‐examined in an attempt to explain its intraseasonal variation and its relation to Rossby wave breaking (RWB). Reanalyses in isentropic coordinates from the National Centers for Environmental Prediction Climate Forecast System for the 1979–2017 period are used to evaluate the relevant features of RWB in the context of waveguide, wave–mean‐flow interaction, and the QBO‐induced meridional circulation. During eQBO, the net extratropical wave forcing is enhanced in early winter with ∼25% increase in upward propagating planetary‐scale Rossby waves (PRWs) of zonal wave‐number 1 (wave‐1). RWB is also enhanced in the lower stratosphere, characterized by convergent anomalies in the subtropics and at high latitudes and strengthened waveguide in between at 20°N–40°N, 350–650 K. In late winter, RWB leads to finite amplitude growth, which hinders upward propagating PRWs. The effect is most significant for zonal wave‐numbers 2 and 3 (wave‐2‐3). During wQBO, RWB in association with wave‐2‐3 is enhanced in the upper stratosphere. Wave absorption/mixing in the surf zone reinforces a stable polar vortex in early to middle winter. A poleward confinement of the extratropical waveguide in the upper stratosphere forces RWB to extend downward around January. A strengthening of upward propagating wave‐2‐3 follows and the polar‐vortex response switches from reinforcement to disturbance around February, thus a sign reversal of the HTE in late winter.

• Rossby wave breaking (RWB) is enhanced in the height regions where the zero‐wind line is shifted into the winter hemisphere and where the QBO‐induced meridional circulation is directed toward the winter pole

• Polar vortex responses differ in terms of the height location of RWB, zonal wave‐number‐dependent disturbances and seasonal development

• Significant increase in wave‐1 occurs when the QBO is in its easterly phase

• A cumulative effect of RWB results in enhanced wave forcing of zonal wave‐numbers 2 and 3 during westerly QBO, which manifests in a sign reversal of the Holton–Tan effect in late winter.