Self-similar mesocrystals form via interface-driven nucleation and assembly.

Crystallization by particle attachment (CPA) is a frequently occurring mechanism of colloidal crystallization that results in hierarchical morphologies1-4. CPA has been exploited to create nanomaterials with unusual properties4-6 and is implicated in the development of complex mineral textures1,7. Oriented attachment7,8-a form of CPA in which particles align along specific crystallographic directions-produces mesocrystals that diffract as single crystals do, although the constituent particles are still discernible2,9. The conventional view of CPA is that nucleation provides a supply of particles that aggregate via Brownian motion biased by attractive interparticle potentials1,9-12. However, mesocrystals often exhibit regular morphologies and uniform sizes. Although many crystal systems form mesocrystals1-9 and individual attachment events have been directly visualized10, how random attachment events lead to well defined, self-similar morphologies remains unknown, as does the role of surface-bound ligands, which are ubiquitous in nanoparticle systems3,9,11. Attempts to understand mesocrystal formation are further complicated in many systems by the presence of precursor nanoparticles with a phase distinct from that of the bulk1,13,14. Some studies propose that such particles convert before attachment15, whereas others attribute conversion to the attachment process itself16 and yet others conclude that transformation occurs after the mesocrystals exceed a characteristic size14,17. Here we investigate mesocrystal formation by iron oxides, which are important colloidal phases in natural environments18,19 and classic examples of systems forming ubiquitous precursor phases and undergoing CPA accompanied by phase transformations15,19-21. Combining in situ transmission electron microscopy (TEM) at 80 degrees Celsius with 'freeze-and-look' TEM, we tracked the formation of haematite (Hm) mesocrystals in the presence of oxalate (Ox), which is abundant in soils, where iron oxides are common. We find that isolated Hm particles rarely appear, but once formed, interfacial gradients at the Ox-covered surfaces drive Hm particles to nucleate repeatedly about two nanometres from the surfaces, to which they then attach, thereby generating mesocrystals. Comparison to natural and synthetic systems suggests that interface-driven pathways are widespread.

Amyloid-like amelogenin nanoribbons template mineralization via a low-energy interface of ion binding sites.

Protein scaffolds direct the organization of amorphous precursors that transform into mineralized tissues, but the templating mechanism remains elusive. Motivated by models for the biomineralization of tooth enamel, wherein amyloid-like amelogenin nanoribbons guide the mineralization of apatite filaments, we investigated the impact of nanoribbon structure, sequence, and chemistry on amorphous calcium phosphate (ACP) nucleation. Using full-length human amelogenin and peptide analogs with an amyloid-like domain, films of ß-sheet nanoribbons were self-assembled on graphite and characterized by in situ atomic force microscopy and molecular dynamics simulations. All sequences substantially reduce nucleation barriers for ACP by creating low-energy interfaces, while phosphoserines along the length of the nanoribbons dramatically enhance kinetic factors associated with ion binding. Furthermore, the distribution of negatively charged residues along the nanoribbons presents a potential match to the Ca­Ca distances of the multi-ion complexes that constitute ACP. These findings show that amyloid-like amelogenin nanoribbons provide potent scaffolds for ACP mineralization by presenting energetically and stereochemically favorable templates of calcium phosphate ion binding and suggest enhanced surface wetting toward calcium phosphates in general.

Uneven Strain Distribution Induces Consecutive Dislocation Slipping, Plane Gliding, and Subsequent Detwinning of Penta-Twinned Nanoparticles.

Twin structures possess distinct physical and chemical properties by virtue of their specific twin configuration. However, twinning and detwinning processes are not fully understood on the atomic scale. Integrating in situ high resolution transmission electron microscopy and molecular dynamic simulations, we find tensile strain in the asymmetrical 5-fold twins of Au nanoparticles leads to twin boundary migration through dislocation sliding (slipping of an atomic layer) along twin boundaries and dislocation reactions at the 5-fold axis under an electron beam. Migration of one or two layers of twin planes is governed by energy barriers, but overall, the total energy, including surface, lattice strain, and twin boundary energy, is relaxed after consecutive twin boundary migration, leading to a detwinning process. In addition, surface rearrangement of 5-fold twinned nanoparticles can aid in the detwinning process.

Unraveling the cross-talk between N6-methyladenosine modification and non-coding RNAs in breast cancer: Mechanisms and clinical implications.

In recent years, breast cancer (BC) has surpassed lung cancer as the most common malignant tumor worldwide and remains the leading cause of cancer death in women. The etiology of BC usually involves dysregulation of epigenetic mechanisms and aberrant expression of certain non-coding RNAs (ncRNAs). N6-methyladenosine (m6A), the most prevalent RNA modification in eukaryotes, widely exists in ncRNAs to affect its biosynthesis and function, and is an important regulator of tumor-related signaling pathways. Interestingly, ncRNAs can also regulate or target m6A modification, playing a key role in cancer progression. However, the m6A-ncRNAs regulatory network in BC has not been fully elucidated, especially the regulation of m6A modification by ncRNAs. Therefore, in this review, we comprehensively summarize the interaction mechanisms and biological significance of m6A modifications and ncRNAs in BC. Meanwhile, we also focused on the clinical application value of m6A modification in BC diagnosis and prognosis, intending to explore new biomarkers and potential therapeutic targets.

Polysulfide Anions [Sx]2- (x = 2, 3, 4, 5): Promising Functional Building Units for Infrared Nonlinear Optical Materials.

Infrared nonlinear optical (IR NLO) materials play significant roles in laser technology. The novel functional building units (FBUs) are of great importance in constructing NLO materials with strong second harmonic generation (SHG). Herein, polysulfide anion [Sx]2- (x = 2, 3, 4, 5) units are investigated on NLO-related properties and structure-performance relationships. Theoretical calculations uncover that the [Sx]2- (x = 2, 3, 4, 5) units are potential IR NLO FBUs with large polarizability anisotropy (δ), hyperpolarizability (ß) and wide HOMO-LUMO gap. Fourteen crystals including [Sx]2- (x = 2, 3, 4, 5) units are calculated and analyzed. The results show that these units can result in a wide IR transmittance range, significant SHG effects, wide band gap Eg (Na2S4: Eg = 3.09 eV), and large birefringence Δn [BaS3 (P21212): Δn = 0.70]. More importantly, it is highlighted that the crystal materials including with [Sx]2- (x = 2, 3, 4, 5) groups are good candidates for the exploration of the outstanding IR NLO materials.

Proton Relay for the Rate Enhancement of Electrochemical Hydrogen Reactions at Heterogeneous Interfaces.

Proton transfer is critically important to many electrocatalytic reactions, and directed proton delivery could open new avenues for the design of electrocatalysts. However, although this approach has been successful in molecular electrocatalysis, proton transfer has not received the same attention in heterogeneous electrocatalyst design. Here, we report that a metal oxide proton relay can be built within heterogeneous electrocatalyst architectures and improves the kinetics of electrochemical hydrogen evolution and oxidation reactions. The volcano-type relationship between activity enhancement and pKa of amine additives confirms this improvement; we observe maximum rate enhancement when the pKa of a proton relay matches the pH of the electrolyte solution. Density-functional-theory-based reactivity studies reveal a decreased proton transfer energy barrier with a metal oxide proton relay. These findings demonstrate the possibility of controlling the proton delivery and enhancing the reaction kinetics by tuning the chemical properties and structures at heterogeneous interfaces.

Single-cell transcriptomics provide insight into metastasis-related subsets of breast cancer.

Breast cancer metastasis is a complex, multi-step process, with high cellular heterogeneity between primary and metastatic breast cancer, and more complex interactions between metastatic cancer cells and other cells in the tumor microenvironment. High-resolution single-cell transcriptome sequencing technology can visualize the heterogeneity of malignant and non-malignant cells in the tumor microenvironment in real time, especially combined with spatial transcriptome analysis, which can directly compare changes between different stages of metastatic samples. Therefore, this study takes single-cell analysis as the first perspective to deeply explore special or rare cell subpopulations related to breast cancer metastasis, systematically summarizes their functions, molecular features, and corresponding treatment strategies, which will contribute to accurately identify, understand, and target tumor metastasis-related driving events, provide a research basis for the mechanistic study of breast cancer metastasis, and provide new clues for its personalized precision treatment.

Lycopene ameliorates aflatoxin B1-induced testicular lesion by attenuating oxidative stress and mitochondrial damage with Nrf2 activation in mice.

Aflatoxin B1 (AFB1) is an extremely hazardous and unavoidable pollutant for cereals and feedstuff. AFB1 can cause testicular lesion, and how to alleviate its testicular toxicity has received much attention in recent years. Lycopene (LYC), a foodborne nutrient derived from red fruits and vegetables, has protective effects against sperm abnormality and testicular lesions. To confirm the beneficial effects and mechanisms of LYC on AFB1-induced testicular lesion, 48 male mice were exposed to 0.75 mg/kg AFB1 or/and 5 mg/kg LYC for consecutive 30 days. Results demonstrated the LYC significantly restored the lesions of testicular microstructure and ultrastructure, and sperm abnormalities in AFB1-exposed mice. Furthermore, LYC effectively attenuated AFB1-induced oxidative stress and mitochondrial damage, including ameliorative mitochondrial structural, and elevated mitochondrial biogenesis for maintaining mitochondrial function. Meanwhile, LYC resisted AFB1-induced mitochondrial-dependent apoptosis. In addition, LYC promoted nuclear factor erythroid 2-related factor 2 (Nrf2) nuclear translocation, and upregulated the Nrf2 signaling pathway. Collectively, our findings demonstrate LYC ameliorates AFB1-induced testicular lesion by attenuating oxidative stress and mitochondrial damage, which is related to the activation of Nrf2.

Parkin-mediated mitophagy protects against aluminum trichloride-induced hippocampal apoptosis in mice via the mtROS-NLRP3 pathway.

Aluminum is a neurotoxic food contaminant. Aluminum trichloride (AlCl3) causes hippocampal mitochondrial damage, leading to hippocampal injury. Damaged mitochondria can release mitochondrial reactive oxygen species (mtROS) and activate nucleotide-binding oligomerization domain-like receptor-containing 3 (NLRP3) inflammasomes and apoptosis. E3 ubiquitin ligase PARK2 (Parkin)-mediated mitophagy can attenuate mitochondrial damage. However, the role of mitophagy in AlCl3-induced mice hippocampal damage and its regulatory mechanism remain elusive. First, C57BL/6 N mice were treated with 0, 44.825, 89.65, and 179.3 mg/kg body weight AlCl3 drinking water for 90 d. Apoptosis, NLRP3-inflammasome activation and mitochondrial damage were increased in AlCl3-induced hippocampal damage. In addition, Parkin-mediated mitophagy peaked in the middle-dose group and was slightly attenuated in the high-dose group. Subsequently, we used wild-type and Parkin knockout (Parkin-/-) mice to investigate the AlCl3-induced hippocampal damage. The results showed that Parkin-/- inhibited mitophagy, and aggravated AlCl3-induced mitochondrial damage, NLRP3-inflammasome activation, apoptosis and hippocampal damage. Finally, we administered MitoQ (mtROS inhibitor) and MCC950 (NLRP3 inhibitor) to AlCl3-treated Parkin-/- mice to investigate the mechanism of Parkin-mediated mitophagy. The results showed that inhibition of mtROS and NLRP3 attenuated hippocampal NLRP3-inflammasome activation, apoptosis, and damage in AlCl3-treated Parkin-/- mice. These findings indicate that Parkin-mediated mitophagy protects against AlCl3-induced hippocampal apoptosis in mice via the mtROS-NLRP3 pathway.

The Plasma Membrane H+ ATPase CsPMA2 Regulates Lipid Droplet Formation, Appressorial Development and Virulence in Colletotrichum siamense.

Plasma membrane H+-ATPases (PMAs) play an important role in the pathogenicity of pathogenic fungi. Lipid droplets are important storage sites for neutral lipids in fungal conidia and hyphae and can be used by plant pathogenic fungi for infection. However, the relationship between plasma membrane H+-ATPase, lipid droplets and virulence remains unclear. Here, we characterized a plasma membrane H+-ATPase, CsPMA2, that plays a key role in lipid droplet formation, appresorial development and virulence in C. siamense. Deletion of CsPMA2 impaired C. siamense conidial size, conidial germination, appressorial development and virulence but did not affect hyphal growth. ΔCsPMA2 increased the sensitivity of C. siamense to phytic acid and oxalic acid. CsPMA2 was localized to lipids on the plasma membrane and intracellular membrane. Deletion of CsPMA2 significantly inhibited the accumulation of lipid droplets and significantly affected the contents of some species of lipids, including 12 species with decreased lipid contents and 3 species with increased lipid contents. Furthermore, low pH can inhibit CsPMA2 expression and lipid droplet accumulation. Overall, our data revealed that the plasma membrane H+-ATPase CsPMA2 is involved in the regulation of lipid droplet formation and affects appressorial development and virulence in C. siamense.

Hyperuricemia induces lipid disturbances by upregulating the CXCL-13 pathway.

The molecular mechanism underlying hyperuricemia-induced lipid metabolism disorders is not clear. The purpose of the current study was to investigate the mechanism of lipid disturbances in a hyperuricemia mice model. RNA-Seq showed that differentially expressed genes (DEGs) in the fatty acid synthesis signaling pathway were mainly enriched and CXCL-13 was significantly enriched in protein-protein interaction networks. Western blotting, Q-PCR, and immunofluorescence results further showed that hyperuricemia upregulated CXCL-13 and disturbed lipid metabolism in vivo and in vitro. Furthermore, CXCL-13 alone also promoted the accumulation of lipid droplets and upregulated the expression of FAS and SREBP1, blocking AMPK signaling and activating the PKC and P38 signaling pathways. Silencing CXCL-13 reversed uric-acid-induced lipid droplet accumulation, which further downregulated FAS and SREBP1 expression, inhibited the p38 and PKC signaling, and activated AMPK signaling. In conclusion, hyperuricemia induces lipid metabolism disorders via the CXCL-13 pathway, making CXCL-13 a key regulatory factor linking hyperuricemia and lipid metabolism disorders. These results may provide novel insights for the treatment of hyperuricemia.NEW & NOTEWORTHY The underlying molecular mechanism of hyperuricemia-induced lipid metabolism disorders is still unclear. The study aimed to investigate the mechanism of lipid disturbance in hyperuricemia mice model. To our knowledge, we proposed for the first time that CXCL-13 may be a key regulator of hyperuricemia and lipid metabolism disorders. These results may provide new insights for the clinical treatment of hyperuricemia.

CsAtf1, a bZIP transcription factor, is involved in fludioxonil sensitivity and virulence in the rubber tree anthracnose fungus Colletotrichum siamense.

In phytopathogenic fungi, the HOG MAPK pathway has roles in osmoregulation, fungicide sensitivity, and other processes. The ATF1/CREB-activating transcription factor Atf1 is a regulator that functions downstream of the HOG MAPK pathway. Here, we identified a gene, designated CsAtf1, that encodes a bZIP transcription factor in Colletotrichum siamense, which is the main pathogen that causes Colletotrichum leaf fall disease in rubber trees in China. CsAtf1 localizes to the nucleus. Its mRNA expression correlates positively with that of CsPbs2 and CsHog1 in the HOG MAPK pathway in response to activator (anisomycin), inhibitor (SB203580) and fludioxonil treatments. The CsAtf1 deletion mutant showed slightly retarded mycelial growth, small conidia, slow spore germination, and abnormal appressorium formation. This mutant showed the increased spore germination rate after fludioxonil treatment and more resistance to the fungicide fludioxonil than did the wild-type fungus. However, unlike deletion of Pbs2 or Hog1, which resulted in greater sensitivity to osmotic stress, the CsAtf1 deletion induced slightly increased resistance to osmotic stress and the cell wall stress response. The ΔCsAtf1 strain also exhibited significantly reduced virulence on rubber tree leaves. These data revealed that CsAtf1 plays a key role in the regulation of fludioxonil sensitivity and in pathogenicity regulation in C. siamense.

Interactive modulations between congruency sequence effects and validity sequence effects.

Sequential modulations have been found in both conflict and spatial orienting tasks. The former is called congruency sequence effects (CSE) and the latter is called validity sequence effects (VSE). Although the two effects have similar phenomenon descriptions, the relationship of the cognitive control mechanisms under the two effects is still unclear. Using a modified attentional network test (ANT), a flanker task and an arrow cueing task are integrated into a single task, which enables the test of the possible interactions between CSE and VSE. Since a confound-minimized design is used, the observed sequence effects cannot be attributed to the feature integration of low-level stimulus features or the contingency learning. It was found that the CSE are only significant when the arrow cue in preceding trial is invalid, and the VSE are only significant when the target letter in preceding trial is congruent with the distractor letters. The findings suggest that the sequential modulations during orienting and executive control of attention networks are highly interacted with each other, and the sequence effects in these networks are possibly controlled by a complex and multifaceted adaptive control mechanism.

Dibutyl phthalate causes MC3T3-E1 cell damage by increasing ROS to promote the PINK1/Parkin-mediated mitophagy.

Dibutyl phthalate (DBP) is a plasticizer widely used in daily production, which causes serious environmental pollution, and damage to brain, liver, kidney, and lung by producing excessive reactive oxygen species (ROS) after entering the body. DBP can also cause skeletal dysplasia, but it is unclear whether ROS is involved. In addition, overproduction of ROS can activate mitophagy, which is an important mechanism for regulating mitochondrial quality and cell homeostasis. In order to investigate whether DBP can damage MC3T3-E1 cells (osteoblast cell line) and whether ROS and mitophagy are involved, DBP toxicity experiment, Parkin gene silencing experiment, and N-acetylcysteine (NAC) intervention experiment were performed on MC3T3-E1 cells in turn. First, we found that DBP caused MC3T3-E1 cell viability decline and osteogenic dysfunction, accompanied by the overproduction of ROS and the activation of mitophagy. Then, we found that silencing Parkin expression alleviated DBP-induced apoptosis and osteogenic dysfunction of MC3T3-E1 cells. In addition, NAC treatment inhibited the PINK1/Parkin-mediated mitophagy and alleviated the apoptosis and osteogenic dysfunction of MC3T3-E1 cells caused by DBP. Our research results showed that DBP could cause MC3T3-E1 cell damage by increasing ROS to promote the PINK1/Parkin-mediated mitophagy.

T-2 toxin-induced femur lesion is accompanied by autophagy and apoptosis associated with Wnt/ß-catenin signaling in mice.

T-2 toxin is one of the most common mycotoxins found in grain foods, animal feed, and other agricultural by-products causing food contamination and health threat. The skeletal system is the main target tissue for T-2 toxin. T-2 toxin exposure is also recognized as a potential contributor to multiple types of bone diseases, including Kashin-Beck disease. However, the mechanisms of T-2 toxin-induced bone toxicity remain unclear. In this study, 60 male C57BL/6 mice were exposed T-2 toxin with 0, 0.5, 1 or 2 mg/kg body weight by intragastric administration for 28 days, respectively. Femora were collected for the detections of femur lesion, bone formation factors, oxidative stress, autophagy, apoptosis, and Wnt/ß-catenin signaling. Our research showed that T-2 toxin caused bone formation disorders, presenting as the reduction of the BMD and femur length, bone structure changes and abnormal bone formation proteins expressions, along with enhanced oxidative stress. Meanwhile, T-2 toxin increased expressions of autophagy-related proteins (Beclin 1, ATG5, p62, and LC3), and promoted apoptosis in mouse femur. Moreover, T-2 toxin suppressed the Wnt/ß-catenin signaling and expressions of downstream target genes. Taken together, our data indicated T-2 toxin-induced femur lesion was accompanied by autophagy and apoptosis, which was associated with Wnt/ß-catenin signaling.

TMT-based quantitative proteomic analysis reveals defense mechanism of wheat against the crown rot pathogen Fusarium pseudograminearum.

BACKGROUND: Fusarium crown rot is major disease in wheat. However, the wheat defense mechanisms against this disease remain poorly understood. RESULTS: Using tandem mass tag (TMT) quantitative proteomics, we evaluated a disease-susceptible (UC1110) and a disease-tolerant (PI610750) wheat cultivar inoculated with Fusarium pseudograminearum WZ-8A. The morphological and physiological results showed that the average root diameter and malondialdehyde content in the roots of PI610750 decreased 3 days post-inoculation (dpi), while the average number of root tips increased. Root vigor was significantly increased in both cultivars, indicating that the morphological, physiological, and biochemical responses of the roots to disease differed between the two cultivars. TMT analysis showed that 366 differentially expressed proteins (DEPs) were identified by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment in the two comparison groups, UC1110_3dpi/UC1110_0dpi (163) and PI610750_3dpi/PI610750_0dpi (203). It may be concluded that phenylpropanoid biosynthesis (8), secondary metabolite biosynthesis (12), linolenic acid metabolites (5), glutathione metabolism (8), plant hormone signal transduction (3), MAPK signaling pathway-plant (4), and photosynthesis (12) contributed to the defense mechanisms in wheat. Protein-protein interaction network analysis showed that the DEPs interacted in both sugar metabolism and photosynthesis pathways. Sixteen genes were validated by real-time quantitative polymerase chain reaction and were found to be consistent with the proteomics data. CONCLUSION: The results provided insight into the molecular mechanisms of the interaction between wheat and F. pseudograminearum.

T-2 toxin causes dysfunction of Sertoli cells by inducing oxidative stress.

T-2 toxin is an inevitable mycotoxin in food products and feeds. It is a proven toxicant impairing the male reproductive system. However, previous studies have concentrated on the toxic effect of T-2 toxin on Leydig cells, with little attention on the Sertoli cell cytotoxicity. Therefore, this study aimed to establish the toxic mechanism of T-2 toxin on Sertoli cells. The Sertoli cell line (TM4 cell) was cultured and exposed to different concentrations of T-2 toxin with/without N-acetyl-L-cysteine (NAC) for 24 h. A CCK-8 assay then measured the cell viability. In addition, the expression of TM4 cell biomarkers (FSHR and ABP) and functional factors (occludin (Ocln), zonula occluden-1 (ZO-1), Connexin 43 (Cx-43), and N-Cadherin (N-cad)) were measured by qRT-PCR and Western blotting. The oxidative stress status (ROS, MDA, CAT, and SOD) and apoptosis rate, including the caspase-9, 8, and 3 activities in TM4 cells, were analyzed. We established that (1): T-2 toxin decreased TM4 cells viability and the half-maximal inhibitory concentration was 8.10 nM. (2): T-2 toxin-induced oxidative stress, evidenced by increased ROS and MDA contents, and inhibited CAT and SOD activities. (3): T-2 toxin inhibited FSHR, ABP, ocln, ZO-1, Cx-43, and N-Cad expressions. (4): T-2 toxin promoted TM4 cell apoptosis and caspase-9, 8, and 3 activities. (5): N-acetyl-L-cysteine relieved oxidative stress, functional impairment, and apoptosis in TM4 cells treated with T-2 toxin. Thus, T-2 toxin induced TM4 cell dysfunction through ROS-induced apoptosis.

Probability of detection of electric vehicles with and without added warning sounds.

Detection performance as a function of distance was measured for 16 subjects who pressed a button upon aurally detecting the approach of an electric vehicle. The vehicle was equipped with loudspeakers that broadcast one of four additive warning sounds. Other test conditions included two vehicle approach speeds [10 and 20 km/h (kph)] and two background noise conditions (55 and 60 dBA). All of the test warning sounds were designed to be compliant with FMVSS 141 proposed regulations in regard to the overall sound pressure levels around the vehicle and in 1/3 octave band levels. Previous work has provided detection results as average vehicle detection distance. This work provides the results as probability of detection (Pd) as a function of distance. The curves provide insight into the false alarm rate when the vehicle is far away from the listeners as well and the Pd at the mean detection distance. Results suggest that, although the test sounds provide an average detection distance that exceeds the National Highway Traffic Safety Administration minimum at the two test speeds, Pd is not always 100% at those distances, particularly at the 10 kph. At the higher speed of 20 kph, the tire-road interaction noise becomes dominant, and the detection range is greatly extended.

Vacancy-Enabled O3 Phase Stabilization for Manganese-Rich Layered Sodium Cathodes.

Manganese-rich layered oxide materials hold great potential as low-cost and high-capacity cathodes for Na-ion batteries. However, they usually form a P2 phase and suffer from fast capacity fade. In this work, an O3 phase sodium cathode has been developed out of a Li and Mn-rich layered material by leveraging the creation of transition metal (TM) and oxygen vacancies and the electrochemical exchange of Na and Li. The Mn-rich layered cathode material remains primarily O3 phase during sodiation/desodiation and can have a full sodiation capacity of ca. 220 mAh g-1 . It delivers ca. 160 mAh g-1 specific capacity between 2-3.8 V with >86 % retention over 250 cycles. The TM and oxygen vacancies pre-formed in the sodiated material enables a reversible migration of TMs from the TM layer to the tetrahedral sites in the Na layer upon de-sodiation and sodiation. The migration creates metastable states, leading to increased kinetic barrier that prohibits a complete O3-P3 phase transition.

[Genome-wide identification, phylogenetic analysis and expression profiling of the MKK gene family in Arabidopsis pumila].

Mitogen-activated protein kinase kinase (MAPKK or MKK) is an important component of the MAPK cascade, which plays important roles in plant growth and development as well as in various stress responses. At present, the MKK gene family has been identified in a variety of plants, but there has been no systematic study in Cruciferous plant Arabidopsis pumila. To explore the evolution and function of the MKK gene family in Arabidopsis pumila, 16 ApMKK genes were identified from the Arabidopsis pumila genome by genome-wide analysis, and they were distributed on 10 chromosomes of Arabidopsis pumila. According to phylogenetic analysis and multiple sequence alignment, these putative genes were divided into five known subfamilies, i.e, Groups A, B, C, D, and E, which includes 5, 2, 4, 3, 2 members, respectively. Evolutionary and syntenic analysis showed that there are seven pairs of duplication genes in Arabidopsis pumila: ApMKK1-1/1-2, ApMKK2-1/2-2, ApMKK3-1/3-2, ApMKK4-1/4-2, ApMKK5-1/5-2, ApMKK9-1/9-2, and ApMKK10-1/10-2. Ka/Ks and Tajima analysis indicated that evolution of ApMKK1-1/1-2 was accelerated after the duplication event. Combining the distribution of cis-element in the promoter region of ApMKKs and the expression profile of ApMKKs in mature leaves, stems, flowers and fruits as well as under salt stress, we found that the expressions of paralogous genes (duplication genes) were tissue-specific and their functions were diversified. The expression patterns of some duplicated genes in tissues were different, but the expression patterns under salt stress were basically the same. These results lay the foundation for analyzing the complex mechanisms of MKK-mediated growth and development and abiotic stress signal transduction pathways in Arabidopsis pumila.