Nitrogen and phosphorus fertilization negatively affects strigolactone production and exudation in sorghum

Strigolactones (SLs) are essential host recognition signals for both root parasitic plants and arbuscular mycorrhizal fungi, and SLs or their metabolites function as a novel class of plant hormones regulating shoot and root architecture. Our previous study indicated that nitrogen (N) deficiency as well as phosphorus (P) deficiency in sorghum enhanced root content and exudation of 5-deoxystrigol, one of the major SLs produced by sorghum. In the present study, we examined how N and P fertilization affects SL production and exudation in sorghum plants subjected to short- (5 days) or long-term (10 days) N or P deficiency and demonstrated their common and distinct features. The root contents and exudation of SLs in the N- or P-deficient sorghum plants grown for 6, 12 or 24 h with or without N or P fertilization were quantified by LC–MS/MS. In general, without fertilization, root contents and exudation of SLs stayed at similar levels at 6 and 12 h and then significantly increased at 24 h. The production of SLs responded more quickly to P fertilization than the secretion of SLs, while regulation of SL secretion began earlier after N fertilization. It is suggested that sorghum plants regulate SL production and exudation when they are subjected to nutrient deficiencies depending on the type of nutrient and degree of deficiency.     

Interplant volatile signaling in willows: revisiting the original talking trees

The importance of interplant volatile signaling in plant–herbivore interactions has been a contentious issue for the past 30 years. We revisit willows as the system in which evidence for interplant signaling was originally found, but then questioned. We established three well-replicated experiments with two willow species (Salix exigua and Salix lemmonii) to address whether the receipt of an interplant signal from a neighboring willow reduces herbivore damage. Additionally we tested whether this signal is volatile in nature, and whether plants signal better to themselves than they do to other individuals. In all three experiments, we found evidence that cues from a damaged neighbor reduce subsequent herbivory experienced by willows. In one experiment, we showed that bagging of clipped tissue, which prevents the exchange of volatile signals, removed the effect of neighbor wounding. This was consistent with results from the other two experiments, in which clipping potted neighbors connected only through airborne volatile cues reduced damage of receivers. In one year, we found evidence that the perception of volatile signals from genetically identical clones was more effective at reducing foliar damage to a neighbor than signals from a genetically different individual. However, this trend was not significant in the following year. In three well-replicated experiments, we found strong evidence for the importance of interplant volatile cues in mediating herbivore interactions with willows.     

Cortical GluK1 kainate receptors modulate scratching in adult mice

Recent investigations into the mechanisms mediating itch transmission have focused on spinal mechanisms, whereas few studies have investigated the role of the cerebral cortex in itch‐related behaviors. Human imaging studies show that several cortical regions are active in correspondence with itch, including the anterior cingulate cortex (ACC). We present here evidence of cortical modulation of pruritogen‐induced scratching behavior. We combine pharmacological, genetic, and electrophysiological approaches to show that cortical GluK1‐containing kainate (KA) receptors are involved in scratching induced by histamine and non‐histamine‐dependent itching stimuli. We further show that scratching corresponds with enhanced excitatory transmission in the ACC through KA receptor modulation of inhibitory circuitry. In addition, we found that inhibiting GluK1‐containing KA receptors in the ACC also reduced behavioral nociceptive responses induced by formalin. Our results reveal a new role of the cortex in pruritogen‐induced scratching.

     

Glu-44 in the Amino-terminal α-Helix of Yeast Vacuolar ATPase E Subunit (Vma4p) Has a Role for VoV1 Assembly

The proton (H⁺) pumping vacuolar-type ATPase (V-ATPase) is a rotary enzyme that plays a pivotal role in forming intracellular acidic compartments in eukaryotic cells. In Saccharomyces cerevisiae, the membrane extrinsic catalytic V₁ and the transmembrane proton-pumping V_o complexes have been shown to reversibly dissociate upon removal of glucose from the medium. However, the basis of this disassembly is largely unknown. In the earlier study, we have found that the amino-terminal α-helical domain between Lys-33 and Lys-83 of yeast E subunit (Vma4p) in the peripheral stalk of the V₁ complex has a role in glucose-dependent V_oV₁ assembly. Results of alanine-scanning mutagenesis within the domain revealed that the Vma4p Glu-44 is a key residue in V_oV₁ disassembly. Biochemical analysis on Vma4p Glu-44 to Ala, Asn, Asp, and Gln substitutions indicated that Glu-44 has a role in V-ATPase catalysis. These results suggest that Glu-44 is one of the key functional residues for subunit interaction in the V-ATPase stalk complex that allows both efficient rotation catalysis and assembly.     

Close Genetic Relationship between Legionella pneumophila Serogroup 1 Isolates from Sputum Specimens and Puddles on Roads,as Determined by Sequence-Based Typing

We investigated the prevalence of Legionella species isolated from puddles on asphalt roads. In addition, we carried out sequence-based typing (SBT) analysis on the genetic relationship between L. pneumophila serogroup 1 (SG 1) isolates from puddles and from stock strains previously obtained from sputum specimens and public baths. Sixty-nine water samples were collected from puddles on roads at 6 fixed locations. Legionella species were detected in 33 samples (47.8%) regardless of season. Among the 325 isolates from puddles, strains of L. pneumophila SG 1, a major causative agent of Legionnaires'' disease, were the most frequently isolated (n = 62, 19.1%). Sixty-two isolates of L. pneumophila SG 1 from puddles were classified into 36 sequence types (STs) by SBT. ST120 and ST48 were identified as major STs. Environmental ST120 strains from puddles were found for the first time in this study. Among the 14 STs of the clinical isolates (n = 19), 4 STs (n = 6, 31.6%), including ST120, were also detected in isolates from puddles on roads, and the sources of infection in these cases remained unclear. The lag-1 gene, a tentative marker for clinical isolates, was prevalent in puddle isolates (61.3%). Our findings suggest that puddles on asphalt roads serve as potential reservoirs for L. pneumophila in the environment.     

Connexin-43 hemichannels contribute to the propagation of μ-calpain-mediated neuronal death in a cortical ablation injury model

We investigated the role of the astrocytic and neuronal hemichannels (HCs) in the spread of cortical neuronal death in a rat cortical injury model. Over time (by 6 h), propidium iodide (PI)-positive cells with labeling either with anti-neuron specific enolase or anti-parvalbumin (indicating GABAnergic interneurons) antibody spread in the deep cortical layers adjacent to the injury and co-localized with activated μ-calpain. Connexin (Cx)-43, glial fibrillary acidic protein (GFAP), activated μ-calpain and α-fodrin breakdown product (FBP) increased post-injury, peaking at 1 h, in the injury and adjacent areas. GFAP-Cx43-positive reactivated astrocytes exhibited similar distribution to the dead neurons. Cx43 and Cx36 primarily comprise HCs in the astrocyte and neuron, respectively. Ethidium bromide (EtBr) uptake was enhanced post-injury, and confirmed in the Cx43- and Cx36-positive cells. A Cx43-HC inhibitor Gap26 prevented the opening of the Cx43-HC and Cx36-HC, μ-calpain activation, α-fodrin proteolysis and death in the deep cortical neurons. Collectively, opening of the astrocytic Cx43-HC and neuronal Cx36-HC would induce the regional spread of cortical neuronal death through μ-calpain activation in the rat brain injury model.