Elevated CO2 causes different growth stimulation, water- and nitrogen-use efficiencies, and leaf ultrastructure responses in two conifer species under intra- and interspecific competition

The continuously increasing atmospheric carbon dioxide concentration ([CO2]) has substantial effects on plant growth, and on the composition and structure of forests. However, how plants respond to elevated [CO2] (e[CO2]) under intra- and interspecific competition has been largely overlooked. In this study, we employed Abies faxoniana Rehder & Wilson and Picea purpurea Mast. seedlings to explore the effects of e[CO2] (700 p.p.m.) and plant-plant competition on plant growth, physiological and morphological traits, and leaf ultrastructure. We found that e[CO2] stimulated plant growth, photosynthesis and nonstructural carbohydrates (NSC), affected morphological traits and leaf ultrastructure, and enhanced water- and nitrogen (N)- use efficiencies in A. faxoniana and P. purpurea. Under interspecific competition and e[CO2], P. purpurea showed a higher biomass accumulation, photosynthetic capacity and rate of ectomycorrhizal infection, and higher water- and N-use efficiencies compared with A. faxoniana. However, under intraspecific competition and e[CO2], the two conifers showed no differences in biomass accumulation, photosynthetic capacity, and water- and N-use efficiencies. In addition, under interspecific competition and e[CO2], A. faxoniana exhibited higher NSC levels in leaves as well as more frequent and greater starch granules, which may indicate carbohydrate limitation. Consequently, we concluded that under interspecific competition, P. purpurea possesses a positive growth and adjustment strategy (e.g. a higher photosynthetic capacity and rate of ectomycorrhizal infection, and higher water- and N-use efficiencies), while A. faxoniana likely suffers from carbohydrate limitation to cope with rising [CO2]. Our study highlights that plant-plant competition should be taken into consideration when assessing the impact of rising [CO2] on the plant growth and physiological performance.Peer reviewe

Human pDCs preferentially sense enveloped hepatitis A virions

Unlike other picornaviruses, hepatitis A virus (HAV) is cloaked in host membranes when released from cells, providing protection from neutralizing antibodies and facilitating spread in the liver. Acute HAV infection is typified by minimal type I IFN responses; therefore, we questioned whether plasmacytoid dendritic cells (pDCs), which produce IFN when activated, are capable of sensing enveloped virions (eHAV). Although concentrated nonenveloped virus failed to activate freshly isolated human pDCs, these cells produced substantial amounts of IFN-α via TLR7 signaling when cocultured with infected cells. pDCs required either close contact with infected cells or exposure to concentrated culture supernatants for IFN-α production. In isopycnic and rate-zonal gradients, pDC-activating material cosedimented with eHAV but not membrane-bound acetylcholinesterase, suggesting that eHAV, and not viral RNA exosomes, is responsible for IFN-α induction. pDC activation did not require virus replication and was associated with efficient eHAV uptake, which was facilitated by phosphatidylserine receptors on pDCs. In chimpanzees, pDCs were transiently recruited to the liver early in infection, during or shortly before maximal intrahepatic IFN-stimulated gene expression, but disappeared prior to inflammation onset. Our data reveal that, while membrane envelopment protects HAV against neutralizing antibody, it also facilitates an early but limited detection of HAV infection by pDCs

Disruption of TLR3 Signaling Due to Cleavage of TRIF by the Hepatitis A Virus Protease-Polymerase Processing Intermediate, 3CD

Toll-like receptor 3 (TLR3) and cytosolic RIG-I-like helicases (RIG-I and MDA5) sense viral RNAs and activate innate immune signaling pathways that induce expression of interferon (IFN) through specific adaptor proteins, TIR domain-containing adaptor inducing interferon-β (TRIF), and mitochondrial antiviral signaling protein (MAVS), respectively. Previously, we demonstrated that hepatitis A virus (HAV), a unique hepatotropic human picornavirus, disrupts RIG-I/MDA5 signaling by targeting MAVS for cleavage by 3ABC, a precursor of the sole HAV protease, 3Cpro, that is derived by auto-processing of the P3 (3ABCD) segment of the viral polyprotein. Here, we show that HAV also disrupts TLR3 signaling, inhibiting poly(I:C)-stimulated dimerization of IFN regulatory factor 3 (IRF-3), IRF-3 translocation to the nucleus, and IFN-β promoter activation, by targeting TRIF for degradation by a distinct 3ABCD processing intermediate, the 3CD protease-polymerase precursor. TRIF is proteolytically cleaved by 3CD, but not by the mature 3Cpro protease or the 3ABC precursor that degrades MAVS. 3CD-mediated degradation of TRIF depends on both the cysteine protease activity of 3Cpro and downstream 3Dpol sequence, but not 3Dpol polymerase activity. Cleavage occurs at two non-canonical 3Cpro recognition sequences in TRIF, and involves a hierarchical process in which primary cleavage at Gln-554 is a prerequisite for scission at Gln-190. The results of mutational studies indicate that 3Dpol sequence modulates the substrate specificity of the upstream 3Cpro protease when fused to it in cis in 3CD, allowing 3CD to target cleavage sites not normally recognized by 3Cpro. HAV thus disrupts both RIG-I/MDA5 and TLR3 signaling pathways through cleavage of essential adaptor proteins by two distinct protease precursors derived from the common 3ABCD polyprotein processing intermediate

Role of Envelopment in the HEV Life Cycle

Hepatitis E virus (HEV), an enterically transmitted hepatotropic virus, was thought to be non-enveloped for decades. However, recent studies have revealed that the virus circulating in the patient’s blood is completely cloaked in host membranes and resistant to neutralizing antibodies. The discovery of this novel enveloped form of HEV has raised a series of questions about the fundamental biology of HEV and the way this virus, which has been understudied in the past, interacts with its host. Here, we review recent advances towards understanding this phenomenon and discuss its potential impact on various aspects of the HEV life cycle and immunity

Sex-specific strategies of nutrient resorption associated with leaf economics in Populus euphratica

There are differences between sexes in physiological and functional traits and possibly in nutrient resorption, particularly in nutrient-poor environments. However, little is known about the extent of nutrient resorption from fine stems and fine roots, and about how nutrient resorption is related to leaf economics in the males and females of dioecious trees. We investigated nutrient resorption of different organs and explored whether nutrient resorption is associated with nutrient conservation traits of leaves (e.g. leaf thickness, leaf mass per area, LMA) in Populus euphratica females and males in four natural forests along the Tarim River, China. Both female and male leaves had the highest N resorption efficiency (NRE), than stems and roots. We found sexual dimorphism in leaf nutrient resorption at Shaya, Luntai and Yuli forest sites, where P. euphratica males had higher leaf NRE than females, whereas females had a higher leaf P resorption efficiency (PRE). Moreover, the different nutrient resorption strategies were related to leaf economics. P. euphratica males possess a conservation strategy with a higher leaf thickness, LMA and leaf vein density, which positively correlated with leaf NRE, while females with higher leaf PRE resorbed disproportionately more P for the reproductive investment. Synthesis. Populus euphratica males possess a conservation strategy with higher leaf NRE, while females have higher leaf PRE for the reproductive investment. Due to spatial sexual segregation across environmental gradients, dioecious plants are especially vulnerable under future climate change. The differences in nutrient uptake and utilization strategies between females and males may result in a situation where one sex is more prone to future climate change than the other one. Such sex-specific nutrient resorption strategies are associated with leaf economics. The present study deepens our understanding of the nutrient balance and adaptation strategies of plants under climate change.Peer reviewe

The unfolded protein response plays dual roles in rice stripe virus infection through fine-tuning the movement protein accumulation.

The movement of plant viruses is a complex process that requires support by the virus-encoded movement protein and multiple host factors. The unfolded protein response (UPR) plays important roles in plant virus infection, while how UPR regulates viral infection remains to be elucidated. Here, we show that rice stripe virus (RSV) elicits the UPR in Nicotiana benthamiana. The RSV-induced UPR activates the host autophagy pathway by which the RSV-encoded movement protein, NSvc4, is targeted for autophagic degradation. As a counteract, we revealed that NSvc4 hijacks UPR-activated type-I J-domain proteins, NbMIP1s, to protect itself from autophagic degradation. Unexpectedly, we found NbMIP1 stabilizes NSvc4 in a non-canonical HSP70-independent manner. Silencing NbMIP1 family genes in N. benthamiana, delays RSV infection, while over-expressing NbMIP1.4b promotes viral cell-to-cell movement. Moreover, OsDjA5, the homologue of NbMIP1 family in rice, behaves in a similar manner toward facilitating RSV infection. This study exemplifies an arms race between RSV and the host plant, and reveals the dual roles of the UPR in RSV infection though fine-tuning the accumulation of viral movement protein

Layered space shift keying modulation over MIMO channels

\u3cp\u3eSpace shift keying (SSK) modulation is an emerging transmission technique for multiple-input multiple-output (MIMO) wireless channels, which exploits the spatial domain to convey information. In this paper, we present a layered space shift keying (LSSK) modulation scheme to fully exploit the spatial domain to transmit information bits, where a layered architecture is developed to achieve spatial multiplexing transmission in an SSK system. Specifically, LSSK leverages the rotated signals predetermined at the transceiver to identify different layers and improve the bit-error-rate (BER) performance. The layered signals are directly generated by the proposed LSSK modulation method with a low computational overhead. Furthermore, we propose a layered-and-joint (LJ) near-optimal detection algorithm based on the layered architecture of LSSK to reduce the detection complexity. In LJ detection, layered detection is performed to find a set of detection candidates for each layer, and then, joint detection is performed with these candidates. We show that the performance of LJ detection is quite close to that of optimal maximum-likelihood detection with significantly reduced detection complexity for high-spectrum-efficiency scenarios. Results demonstrate that the proposed LSSK scheme substantially improves the spectrum efficiency of an SSK system and outperforms other existing MIMO schemes.\u3c/p\u3

NSvc4 Encoded by Rice Stripe Virus Targets Host Chloroplasts to Suppress Chloroplast-Mediated Defense

Our previous research found that NSvc4, the movement protein of rice stripe virus (RSV), could localize to the actin filaments, endoplasmic reticulum, plasmodesmata, and chloroplast, but the roles of NSvc4 played in the chloroplast were opaque. Here, we confirm the accumulation of NSvc4 in the chloroplasts and the N-terminal 1–73 amino acids of NSvc4 are sufficient to localize to chloroplasts. We provide evidence to show that chloroplast-localized NSvc4 can impair the chloroplast-mediated immunity. Expressing NSvc4 in Nicotiana benthamiana leaves results in the decreased expression of defense-related genes NbPR1, NbPR2, and NbWRKY12 and the inhibition of chloroplast-derived ROS production. In addition, generation of an infectious clone of potato virus X (PVX) carrying NSvc4 facilitates PVX infection in N. benthamiana plants. Moreover, we identify two chloroplast-related host factors, named NbGAPDH-A and NbPsbQ1, both of which can interact with NSvc4. Knockdown of NbGAPDH-A or NbPsbQ1 can both promote RSV infection. Our results decipher a detailed function of NSvc4 in the chloroplast