Genome-wide identification, classification, and expression analysis of heat shock transcription factor family in switchgrass (Panicum virgatum L.).

Switchgrass is one of the most promising bioenergy crops and is generally cultivated in arid climates and poor soils. Heat shock transcription factors (Hsfs) are key regulators of plant responses to abiotic and biotic stressors. However, their role and mechanism of action in switchgrass have not been elucidated. Hence, this study aimed to identify the Hsf family in switchgrass and understand its functional role in heat stress signal transduction and heat tolerance by using bioinformatics and RT-PCR analysis. Forty-eight PvHsfs were identified and divided into three main classes based on their gene structure and phylogenetic relationships: HsfA, HsfB, and HsfC. The results of the bioinformatics analysis showed a DNA-binding domain (DBD) at the N-terminal in PvHsfs, and they were not evenly distributed on all chromosomes except for chromosomes 8 N and 8 K. Many cis-elements related to plant development, stress responses, and plant hormones were identified in the promoter sequence of each PvHsf. Segmental duplication is the primary force underlying Hsf family expansion in switchgrass. The results of the expression pattern of PvHsfs in response to heat stress showed that PvHsf03 and PvHsf25 might play critical roles in the early and late stages of switchgrass response to heat stress, respectively, and HsfB mainly showed a negative response to heat stress. Ectopic expression of PvHsf03 in Arabidopsis significantly increased the heat resistance of seedlings. Overall, our research lays a notable foundation for studying the regulatory network in response to deleterious environments and for further excavating tolerance genes in switchgrass.

Comprehensive Transcriptomic and Metabolic Profiling of Agrobacterium-tumefaciens-Infected Immature Wheat Embryos.

The transformation efficiency (TE) was improved by a series of special chemical and physical methods using immature embryos from the cultivar Fielder, with the PureWheat technique. To analyze the reaction of immature embryos infected, which seemed to provide the necessary by Agrobacterium tumefaciens in PureWheat, a combination of scanning electron microscopy (SEM), complete transcriptome analysis, and metabolome analysis was conducted to understand the progress. The results of the SEM analysis revealed that Agrobacterium tumefaciens were deposited under the damaged cortex of immature embryos as a result of pretreatment and contacted the receptor cells to improve the TE. Transcriptome analysis indicated that the differentially expressed genes were mainly enriched in phenylpropanoid biosynthesis, starch and sucrose metabolism, plant-pathogen interaction, plant hormone signal transduction, and the MAPK (Mitogen-activated protein kinase) signaling pathway. By analyzing the correlation between differentially expressed genes and metabolites, the expression of many genes and the accumulation of metabolites were changed in glucose metabolism and the TCA cycle (Citrate cycle), as well as the amino acid metabolism; this suggests that the infection of wheat embryos with Agrobacterium is an energy-demanding process. The shikimate pathway may act as a hub between glucose metabolism and phenylpropanoid metabolism during Agrobacterium infection. The downregulation of the F5H gene and upregulation of the CCR gene led to the accumulation of lignin precursors through phenylpropanoid metabolism. In addition, several metabolic pathways and oxidases were found to be involved in the infection treatment, including melatonin biosynthesis, benzoxazinoid biosynthesis, betaine biosynthesis, superoxide dismutase, and peroxidase, suggesting that wheat embryos may be under the stress of Agrobacterium and, thus, undergo an oxidative stress response. These findings explore the physiological and molecular changes of immature embryos during the co-culture stage of the PureWheat technique and provide insights for Agrobacterium-mediated transgenic wheat experiments.

The THO/TREX Complex Component RAE2/TEX1 Is Involved in the Regulation of Aluminum Resistance and Low Phosphate Response in Arabidopsis.

The C2H2-type zinc finger transcription factor SENSITIVE TO PROTON RHIZOTOXICITY 1 (STOP1) plays a critical role in aluminum (Al) resistance and low phosphate (Pi) response mainly through promoting the expression of the malate transporter-encoding gene ARABIDOPSIS THALIANA ALUMINUM ACTIVATED MALATE TRANSPORTER 1 (AtALMT1). We previously showed that REGULATION OF ATALMT1 EXPRESSION 3 (RAE3/HPR1), a core component of the THO/TREX complex, is involved in the regulation of nucleocytoplasmic STOP1 mRNA export to modulate Al resistance and low Pi response. Here, we report that RAE2/TEX1, another core component of the THO complex, is also involved in the regulation of Al resistance and low Pi response. Mutation of RAE2 reduced the expression of STOP1-downstream genes, including AtALMT1. rae2 was less sensitive to Al than rae3, which was consistent with less amount of malate secreted from rae3 roots than from rae2 roots. Nevertheless, low Pi response was impaired more in rae2 than in rae3, suggesting that RAE2 also regulates AtALMT1-independent pathway to modulate low Pi response. Furthermore, unlike RAE3 that regulates STOP1 mRNA export, mutating RAE2 did not affect STOP1 mRNA accumulation in the nucleus, although STOP1 protein level was reduced in rae2. Introduction of rae1 mutation into rae2 mutant background could partially recover the deficient phenotypes of rae2. Together, our results demonstrate that RAE2 and RAE3 play overlapping but distinct roles in the modulation of Al resistance and low Pi response.

Optical properties of a waveguide-mediated chain of randomly positioned atoms.

We theoretically study the optical properties of an ensemble of two-level atoms coupled to a one-dimensional waveguide. In our model, the atoms are randomly located in the lattice sites along the one-dimensional waveguide. The results reveal that the optical transport properties of the atomic ensemble are influenced by the lattice constant and the filling factor of the lattice sites. We also focus on the atomic mirror configuration and quantify the effect of the inhomogeneous broadening in atomic resonant transition on the scattering spectrum. Furthermore, we find that initial bunching and persistent quantum beats appear in photon-photon correlation function of the transmitted field, which are significantly changed by the filling factor of the lattice sites. With great progress to interface quantum emitters with nanophotonics, our results should be experimentally realizable in the near future.

Mutation of HPR1 encoding a component of the THO/TREX complex reduces STOP1 accumulation and aluminium resistance in Arabidopsis thaliana.

C2H2-type zinc finger transcription factor sensitive to proton rhizotoxicity 1 (STOP1) plays an essential role in aluminium (Al) resistance in Arabidopsis thaliana by controlling the expression of a set of Al-resistance genes, including the malate transporter-encoding gene A. thaliana aluminium activated malate transporter 1 (AtALMT1) that is critically required for Al resistance. STOP1 is suggested to be modulated by Al at post-transcriptional and/or post-translational levels. However, the underlying molecular mechanisms remain to be demonstrated. We carried out a forward genetic screen on an ethyl methanesulphonate mutagenized population, which contains the AtALMT1 promoter-driven luciferase reporter gene (pAtALMT1:LUC), and identified hyperrecombination protein 1 (HPR1), which encodes a subunit of the THO/TREX complex. We investigate the effect of hpr1 mutations on the expression of Al-resistance genes and Al resistance, and we also examined the regulatory role of HPR1 in nuclear messenger RNA (mRNA) and protein accumulation of STOP1 gene. Mutation of HPR1 reduces the expression of STOP1-regulated genes and the associated Al resistance. The hpr1 mutations increase STOP1 mRNA retention in the nucleus and consequently decrease STOP1 protein abundance. Mutation of regulation of AtALMT1 expression 1 (RAE1) that mediates STOP1 degradation in the hpr1 mutant background can partially rescue the deficient phenotypes of hpr1 mutants. Our results demonstrate that HPR1 modulates Al resistance partly through the regulation of nucleocytoplasmic STOP1 mRNA export.

F-box protein RAE1 regulates the stability of the aluminum-resistance transcription factor STOP1 in Arabidopsis.

Aluminum (Al) toxicity is a major factor limiting crop production on acid soils, which represent over 30% of the world's arable land. Some plants have evolved mechanisms to detoxify Al. Arabidopsis, for example, secretes malate via the AtALMT1 transporter to chelate and detoxify Al. The C2H2-type transcription factor STOP1 plays a crucial role in Al resistance by inducing the expression of a set of genes, including AtALMT1 Here, we identify and characterize an F-box protein-encoding gene regulation of Atalmt1 expression 1 (RAE1) that regulates the level of STOP1. Mutation and overexpression of RAE1 increases or decreases the expression of AtALMT1 and other STOP1-regulated genes, respectively. RAE1 interacts with and promotes the degradation of STOP1 via the ubiquitin-26S proteasome pathway, while Al stress promotes the accumulation of STOP1. We find that STOP1 up-regulates RAE1 expression by directly binding to the RAE1 promoter, thus forming a negative feedback loop between STOP1 and RAE1. Our results demonstrate that RAE1 influences Al resistance through the ubiquitination and degradation of STOP1.

The Cell Cycle Checkpoint Regulator ATR Is Required for Internal Aluminum Toxicity-Mediated Root Growth Inhibition in Arabidopsis.

Aluminum (Al) can target multiple sites of root cells for toxicity, including the cell wall, the plasma membrane and symplastic components. Previous work revealed that the cell cycle checkpoint regulator (ATR) Ataxia Telangiectasia-mutated and Rad3-related is required for Al toxicity-induced root growth inhibition in als3 and that the symplastic component DNA is an important target site of Al for the toxicity. However, whether monitoring DNA integrity through ATR-regulated pathway is required for Al-induced root growth inhibition in other Al-sensitive mutants remains unknown. In this study, we demonstrated that the atr mutation could also rescue the Al hypersensitivity and Al-induced cell cycle arrest in star1, which supports the hypothesis that ALS3 and STAR1 function together to be involved in the detoxification of Al in Arabidopsis. However, mutation of ATR could not rescue the Al-sensitive phenotype of almt1 or stop1, both of which are defective in external detoxification mechanisms of Al. We further showed that the Al hypersensitivity and Al-induced quiescent center (QC) differentiation in als1 could also be rescued by the atr mutation. Therefore, our results suggest that ATR-regulated pathway is involved in the modulation of internal Al toxicity-mediated root growth inhibition in Arabidopsis.

Corrigendum: The Cell Cycle Checkpoint Regulator ATR Is Required for Internal Aluminum Toxicity-Mediated Root Growth Inhibition in Arabidopsis.

[This corrects the article on p. 118 in vol. 9, PMID: 29491872.].

Graphene Q-switched eye-safe Nd:Y(3)A(l5)O(12) ceramic dual-wavelength laser.

With graphene as a saturable absorber, the efficient and stable 1.4 µm dual-wavelength operation of Nd:YAG ceramic laser is demonstrated. A maximum total average output power of 601 mW is obtained under the pump power of 22.3 W, corresponding to an optical-optical conversion efficiency of 2.7%. The minimum pulse width and the highest pulse repetition rate are 470 ns and 101 kHz, respectively.

[Immune protection of recombinant membrane protein against Taenia multiceps larvae in sheep].

OBJECTIVE: To investigate the immune protection of the recombinant membrane protein(45M) against larvae of Taenia multiceps in sheep. METHODS: Twelve sheep were randomly divided into immune group and control group, and each sheep was immunized four times (three weeks interval) respectively with 50 microg recombinant 45M or GST emulsified with adjuvant. Serum samples were collected at pre-immunization and certain time after immunization, and were analyzed for IgG and IgM by ELISA. At the 105th day after the final inoculation, each sheep was orally challenged by 5000 eggs of T. multiceps. Two weeks after infection, the sheep were sacrificed, serum samples were collected, and number of cysts in brain tissue was counted. Activated oncospheres were cultured with 10% sera of immune group or control group, and observed by light microscopy. RESULTS: The mean number of cysts was 1.5, and the average diameter of the cysts was 2.2 mm. Compared with control group, the reduction rate of cysts in immunized sheep was 68.9%. At the 72th hour after culture with serum of immunized sheep, about 90% oncospheres were killed by antiserum, and the oncospheres began to shrink or expand, and internal structure became fuzzy. ELISA showed that after final immunization (the 9th week), the levels of IgG in sera of immune group (2.32+/-0.76) were significantly higher than those of the control (0.70+/-0.42) (t=4.47, P<0.01). At the 24th week the levels of IgG and IgM in sera of immune group (1.53+/- 0.81, 0.90+/-0.26) were significantly higher than those of the control (0.64+/-0.43, 0.43+/-0.15) (P<0.01). CONCLUSION: The recombinant 45M can induce certain humoral immune response.