Evaluation of drought stress level in Sargent's cherry (Prunus sargentii Rehder) using photosynthesis and chlorophyll fluorescence parameters and proline content analysis.

Sargent's cherry trees (Prunus sargentiiRehder) are widely planted as an ornamental, climate change-sensing species. This study investigated changes in the soil moisture content, fresh weight, photosynthesis and chlorophyll fluorescence properties, and the chlorophyll and proline content of four-year-old P. sargentii seedlings after 30 days of drought stress. In the trees subjected to drought stress treatment, soil moisture content decreased, and the fresh weight of the aboveground part of the plant decreased. However, there was no significant difference in the root growth of the dried plants. Among the photosynthesis parameters, Pn MAX, E and gs showed a significant (p  <  0.001) decrease after 15 days in dry-stressed seedlings, but there was no difference between treatments in WUE until 20 days, and there was a significant (p  <  0.001) difference after 24 days. Chlorophyll fluorescence parameters, Fv/Fm, ΦPSII, Rfd, NPQ, and Pn MAX, also increased after 10 days in dry-stressed seedlings, but these changes did not reach statistical significance compared to the control treatment. These results may suggest that drought stress highly correlates with photosynthesis and chlorophyll fluorescence parameters. Chlorophyll content also significantly decreased in the seedlings under drought stress compared with the control treatment. The proline content decreased until the 10th day of drought stress treatment and increased after the 15th day, showing an increase of 10.9% on the 15th day and 57.1% on the 30th day, compared to the control treatment. These results suggest that photosynthesis, chlorophyll fluorescence parameters, and proline content can be used to evaluate drought stress in trees. The results of this study can contribute to the management of forests, such as the irrigation of trees when pore control ability and photosynthesis ability decrease.

TMPRSS11a is a novel age-altered, tissue specific regulator of migration and wound healing.

Aging is a gradual biological process characterized by a decrease in cellular and organism functions. Aging-related processes involve changes in the expression and activity of several proteins. Here, we identified the transmembrane protease serine 11a (TMPRSS11a) as a new age-specific protein that plays an important role in skin wound healing. TMPRSS11a levels increased with age in rodent and human skin and gingival samples. Strikingly, overexpression of TMPRSS11a decreased cell migration and spreading, and inducing cellular senescence. Mass spectrometry, bioinformatics, and functional analyses revealed that TMPRSS11a interacts with integrin ß1 through an RGD sequence contained within the C-terminal domain and that this motif was relevant for cell migration. Moreover, TMPRSS11a was associated with cellular senescence, as shown by overexpression and downregulation experiments. In agreement with tissue-specific expression of TMPRSS11a, shRNA-mediated downregulation of this protein improved wound healing in the skin, but not in the skeletal muscle of old mice, where TMPRSS11a is undetectable. Collectively, these findings indicate that TMPRSS11a is a tissue-specific factor relevant for wound healing, which becomes elevated with aging, promoting cellular senescence and inhibiting cell migration and skin repair.

Tyrosine Phosphorylation of the Kv2.1 Channel Contributes to Injury in Brain Ischemia.

In brain ischemia, oxidative stress induces neuronal apoptosis, which is mediated by increased activity of the voltage-gated K+ channel Kv2.1 and results in an efflux of intracellular K+. The molecular mechanisms underlying the regulation of Kv2.1 and its activity during brain ischemia are not yet fully understood. Here this study provides evidence that oxidant-induced apoptosis resulting from brain ischemia promotes rapid tyrosine phosphorylation of Kv2.1. When the tyrosine phosphorylation sites Y124, Y686, and Y810 on the Kv2.1 channel are mutated to non-phosphorylatable residues, PARP-1 cleavage levels decrease, indicating suppression of neuronal cell death. The tyrosine residue Y810 on Kv2.1 was a major phosphorylation site. In fact, cells mutated Y810 were more viable in our study than were wild-type cells, suggesting an important role for this site during ischemic neuronal injury. In an animal model, tyrosine phosphorylation of Kv2.1 increased after ischemic brain injury, with an observable sustained increase for at least 2 h after reperfusion. These results demonstrate that tyrosine phosphorylation of the Kv2.1 channel in the brain may play a critical role in regulating neuronal ischemia and is therefore a potential therapeutic target in patients with brain ischemia.

Characteristics of TAA-ZnS Buffer Layer by Addition of Sodium Citrate for CIGS Thin Film Solar Cell.

Zinc Sulfide (ZnS) is an environmentally friendly material with a wide bandgap (Eg = 3.7 eV) comparable to that of cadmium sulfide (CdS) (2.4 eV), which is conventionally used as buffer layer in Cu(In,Ga)Se2 (CIGS) thin film solar cells. Conventional ZnS buffer layers are manufactured using thiourea, and, these layers possess a disadvantage in that their deposition rate is lower than that of CdS buffer layers. In this paper, thioacetamide (TAA) was used as a sulfur precursor instead of thiourea to increase the deposition rate. However, the ZnS thin films deposited with TAA exhibited a higher roughness than the ZnS thin films deposited with thiourea. Sodium citrate was therefore added to increase the uniformity and decrease the roughness of the former ZnS thin films. When sodium citrate was used, the thin films demonstrated a high transmittance via the controlled generation of particles. In the case of TAA-ZnS thin films doped with a sodium citrate concentration of 0.04 M, the granules on the surface disappeared and these thin films were denser than the TAA-ZnS thin films deposited with a lower sodium citrate concentration. It is considered that the rate of the ion-by-ion reaction increased due to the addition of sodium citrate, thereby resulting in a uniform thin film. Consequently, TAA-ZnS thin films with thicknesses of approximately 40 nm and high transmittances of 83% were obtained when a sodium citrate concentration of 0.04 M was used.

Changes in Bacterial Community Structure and Enriched Functional Bacteria Associated With Turfgrass Monoculture.

There is increasing attention being paid to utilizing microbial communities to improve plant health while reducing management inputs. Thus, the objectives of this research were to assess changes in the rhizosphere bacterial community structure associated with long-term turfgrass monoculture and to demonstrate the feasibility of using functional bacteria as beneficial biocontrol agents. Large patch disease, caused by the fungal pathogen Rhizoctonia solani AG2-2, is a significant threat to turfgrass cultivation. Rhizosphere samples were collected from 2-, 13- and 25-year turfgrass (Zoysia japonica) monocultures. The 13-year monoculture field had a higher pathogen population density than both the 2- and 25-year monoculture fields. Analyses of the rhizosphere bacterial communities revealed that Streptomyces was dominant in the 2-year field and Burkholderia was enriched in the 25-year field. Based on the culturable rhizosphere bacteria, Streptomyces neyagawaensis J6 and Burkholderia vietnamiensis J10 were obtained from the 2- and 25-year fields, respectively. Application of S. neyagawaensis J6 and B. vietnamiensis J10 led to excellent inhibition of large patch disease as well as enhanced tolerance against drought and temperature stresses. The results showed that the selected bacteria could be developed as biocontrol and abiotic stress tolerance agents for turfgrass cultivation.

Foxa2 and Nurr1 synergistically yield A9 nigral dopamine neurons exhibiting improved differentiation, function, and cell survival.

Effective dopamine (DA) neuron differentiation from neural precursor cells (NPCs) is prerequisite for precursor/stem cell-based therapy of Parkinson's disease (PD). Nurr1, an orphan nuclear receptor, has been reported as a transcription factor that can drive DA neuron differentiation from non-dopaminergic NPCs in vitro. However, Nurr1 alone neither induces full neuronal maturation nor expression of proteins found specifically in midbrain DA neurons. In addition, Nurr1 expression is inefficient in inducing DA phenotype expression in NPCs derived from certain species such as mouse and human. We show here that Foxa2, a forkhead transcription factor whose role in midbrain DA neuron development was recently revealed, synergistically cooperates with Nurr1 to induce DA phenotype acquisition, midbrain-specific gene expression, and neuronal maturation. Thus, the combinatorial expression of Nurr1 and Foxa2 in NPCs efficiently yielded fully differentiated nigral (A9)-type midbrain neurons with clearly detectable DA neuronal activities. The effects of Foxa2 in DA neuron generation were observed regardless of the brain regions or species from which NPCs were derived. Furthermore, DA neurons generated by ectopic Foxa2 expression were more resistant to toxins. Importantly, Foxa2 expression resulted in a rapid cell cycle exit and reduced cell proliferation. Consistently, transplantation of NPCs transduced with Nurr1 and Foxa2 generated grafts enriched with midbrain-type DA neurons but reduced number of proliferating cells, and significantly reversed motor deficits in a rat PD model. Our findings can be applied to ongoing attempts to develop an efficient and safe precursor/stem cell-based therapy for PD.

Orphan nuclear receptor Nurr1 induces neuron differentiation from embryonic cortical precursor cells via an extrinsic paracrine mechanism.

Nurr1 is an orphan nuclear receptor-type transcription factor (TF) that plays critical roles in midbrain dopamine neuron development. This study demonstrated a novel role for Nurr1 in neuronal/astrocytic differentiation of neural precursor (NP) cells isolated from rat embryonic cortices: overexpression of this TF promoted NP cell differentiation towards neurons at the expense of astrocytic differentiation. Single cell-based lineage analyses and experiments using co-cultures revealed that Nurr1 elicited its neurogenic role in an extrinsic paracrine manner. We defined diffusible factors and downstream neurogenic TFs responsible for the Nurr1-mediated neuronal differentiation.