Comparative transcriptome profiling reveals the key genes and molecular mechanisms involved in rice under blast infection.

The aim of this study was to analyze the resistance genes and molecular mechanisms involved in rice blast infection. The contents of seven hormones and eight biochemical indicators in the leaves and spikes were at dynamic levels after inoculation with rice blast strains over time. The mRNA and protein expression of the six genes were consistent with the transcriptome analysis results.

Impairment of ovarian follicular development caused by titanium dioxide nanoparticles exposure involved in the TGF-β/BMP/Smad pathway.

Titanium dioxide nanoparticles (TiO NPs) have been shown to induce reproductive system damages in animals. To better underline how TiO NPs act in reproductive system, female mice were exposed to 2.5, 5, or 10 mg/kg TiO NPs by gavage administration for 60 days, the ovary injuries, follicle stimulating hormone (FSH) and luteinizing hormone (LH) levels as well as ovarian follicular development-related molecule expression were investigated.

Mutation in Affects Cadmium and Micronutrient Metal Accumulation in Rice.

Micronutrient metals, such as Mn, Cu, Fe, and Zn, are essential heavy metals for plant growth and development, while Cd is a nonessential heavy metal that is highly toxic to both plants and humans. Our understanding of the molecular mechanisms underlying Cd and micronutrient metal accumulation in plants remains incomplete. Here, we show that , an -like () family gene in , is preferentially expressed in the root and encodes a protein localized to the cell membrane.

Damage to the Blood Brain Barrier Structure and Function from Nano Titanium Dioxide Exposure Involves the Destruction of Key Tight Junction Proteins in the Mouse Brain.

Numerous studies have proven that nano titanium dioxide (nano TiO₂) can accumulate in animal brains, where it damages the blood brain barrier (BBB); however, whether this process involves destruction of tight junction proteins in the mouse brain has not been adequately investigated. In this study, mice were exposed to nano TiO₂ for 30 consecutive days, and then we used transmission electron microscopy to observe the BBB ultrastructure and the Evans blue assay to evaluate the permeability of the BBB. Our data suggested that nano TiO₂ damaged the BBB ultrastructure and increased BBB permeability.

Molecular mechanism of mice gastric oxidative damage induced by nanoparticulate titanium dioxide.

Background: Nanoparticulate titanium dioxide (Nano-TiO) has been widely used in food industry, and it has been demonstrated to have adverse effects on mice and human stomach, but its mechanism is rarely concerned. The aim of this study is to determine the effects of nano-TiO on the stomach and confirm the role of oxidative stress and apoptosis in the mice gastric damage caused by nano-TiO, as well as its molecular mechanisms.

Methods: Mice were continuously exposed to nano-TiO with 1.

PRD1, a homologous recombination initiation factor, is involved in spindle assembly in rice meiosis.

The bipolar spindle structure in meiosis is essential for faithful chromosome segregation. PUTATIVE RECOMBINATION INITIATION DEFECT 1 (PRD1) previously has been shown to participate in the formation of DNA double strand breaks (DSBs). However, the role of PRD1 in meiotic spindle assembly has not been elucidated.

Molecular mechanisms associated with oxidative damage in the mouse testis induced by LaCl.

China is the world's largest rare earth producer and exporter, previous studies have shown that rare earth elements can cause oxidative damage in animal testis. However, the molecular mechanisms underlying these observations have yet to be elucidated. In this paper, male mice were fed with different doses (10, 20, and 40 mg/kg BW) of LaCl for 90 consecutive days, regulatory role of nuclear factor erythroid-2 related factor 2 (Nrf-2)/antioxidant response element (ARE) pathway in testicular oxidative stress induced by LaCl were investigated.

Nanostructured Titanium Dioxide (TiO₂) Reduces Sperm Concentration Involving Disorder of Meiosis and Signal Pathway.

Nano-titanium dioxide (nano-TiO₂) has been widely used in food and cosmetic industries, and the medical sector. However, nano-TiO₂ is potentially toxic to the reproductive system. Previous research has shown that nano-TiO₂ can reduce sperm concentration but do not yet known whether this effect occurs because of dysfunctional meiosis in spermatogenic cells.

Liver Inflammation and Fibrosis Induced by Long-Term Exposure to Nano Titanium Dioxide (TiO₂) Nanoparticles in Mice and Its Molecular Mechanism.

Titanium dioxide (TiO₂) and nano-sized titanium dioxide (nano-TiO₂), which are used in food production, may be harmful to the body. Long-term exposure to nano-TiO₂ can lead to hepatic injury; however, the effect of nano-TiO₂ on liver fibrosis and the underlying mechanism remain unclear. The TGF-/Smad/MAPK/Wnt signaling pathway is important for tissue fibrosis.

Targeted Mutagenesis of the Rice -Like Gene Family Using the CRISPR/Cas9 System Reveals OsFWL4 as a Regulator of Tiller Number and Plant Yield in Rice.

The -like () genes encode cysteine-rich proteins with a placenta-specific 8 domain. They play roles in cell division and organ size control, response to rhizobium infection, and metal ion homeostasis in plants. Here, we target eight rice genes using the CRISPR/Cas9 system delivered by -mediated transformation.

Respiratory exposure to nano-TiO induces pulmonary toxicity in mice involving reactive free radical-activated TGF-β/Smad/p38MAPK/Wnt pathways.

Numerous studies have shown that lung injury can be caused by respiratory exposure to nanoparticulate titanium dioxide (nano-TiO ), but whether pulmonary inflammation and fibrosis are related to the activation of the TGF-β/Smad/p38MAPK/Wnt pathways remains unclear. In this study, mice were administrated nano-TiO by nasal instillation for nine consecutive months, and the molecular mechanisms of nano-TiO on the pulmonary toxicity of mice were examined. The findings suggested that nano-TiO caused pneumonia and pulmonary fibrosis.

Nanoparticulate TiO₂ Induced Suppression of Spermatogenesis is Involved in Regulatory Dysfunction of the cAMP-CREB/CREM Signaling Pathway in Mice.

Long-term exposure to nanoparticulate titanium dioxide (nano-TiO₂) is known to cause reductions of sperm numbers and quality in animals, and the cAMP-dependent signaling pathway has been demonstrated to play a key role in regulating spermatogenesis. However, whether the suppression of spermatogenesis induced by nano-TiO₂ is related to regulatory disturbances of the cAMP-CREB/CREM signaling pathway is not well investigated. In the current study, male mice were exposed to nano-TiO₂ at doses of 1.

Maternal Exposure to Nanoparticulate Titanium Dioxide Causes Inhibition of Hippocampal Development Involving Dysfunction of the Rho/NMDAR Signaling Pathway in Offspring.

Numerous studies have suggested that nano-TiO₂ can be translocated to the brain via the placental barrier and blood brain barrier, leading to brain damage and cognitive impairment in both mice and rat offspring. The mechanism of nanoTiO₂-induced neurotoxicity is still unclear, as is its role in the inhibition of hippocampal development. In this experiment, nano-TiO₂ was employed to investigate whether the inhibition of the hippocampal development of mice offspring involved the alterations in the Rho signaling pathway following consecutive gavage of female mice between 7-21 days postpartum.

Retardation of Axonal and Dendritic Outgrowth Is Associated with the MAPK Signaling Pathway in Offspring Mice Following Maternal Exposure to Nanosized Titanium Dioxide.

Exposure to nanosized titanium oxide (nano-TiO) has been proven to suppress brain growth in mouse offspring; however, whether retardation of axonal or dendritic outgrowth is associated with activation of the mitogen-activated protein kinase (MAPK) pathway remains unclear. In the present study, pregnant mice were exposed to nano-TiO at 1.25, 2.

Suppression of ovarian follicle development by nano TiO is associated with TGF-β-mediated signaling pathways.

Nanoparticulate titanium dioxide (nano TiO ) is extensively applied in biological tissue engineering materials, food additives, cosmetics, and sunscreens. Numerous studies to date have demonstrated that nano TiO penetrates through the digestive system and possibly the blood circulation, leading to accumulation in the ovary and consequent reproductive toxicity. However, the mechanisms underlying the toxic effects of nano TiO on the female reproductive system remain to be established.

Wnt Pathway-Mediated Nano TiO₂-Induced Toxic Effects on Rat Primary Cultured Sertoli Cells.

Nanosized titanium dioxide (Nano TiO₂) has been widely used in daily lives, medicine, industry, and caused the potential reproduction toxicity for animals and human, however, the underlying molecular mechanisms for the reproductive toxicity of nano TiO₂ are still largely unclear. In the present study, when primary cultured rat Sertoli cells (SCs) were exposed to nano TiO₂, cell injury and alterations in wingless related MMTV integration site (Wnt) pathway-related factors including Wnt1, Wnt3a, Wnt5a, Wnt11, -catenin, and p-GSK-3 expression were investigated. The results suggested that nano TiO₂ could be translocated to cytoplasm or nucleus, and decreased cell viability, and impaired morphological structures of SCs, induced apoptosis and dead of primary cultured rat SCs.

Nano-TiO Inhibits Development of the Central Nervous System and Its Mechanism in Offspring Mice.

Nano titanium dioxide (Nano-TiO) has been applied in food packaging systems and food additives, but it may cause potential neurotoxicity for human and animals. In our study, the effects of nano-TiO exposure during pregnancy/lactation on the development of the central nervous system in offspring mice were examined and its molecular mechanism involving Rho family was investigated. Our findings showed that pregnancy/lactation exposure to nano-TiO resulted in thinning of cerebral and cerebellar cortex, decrease in number of neurons per unit area of cerebrum, edema and nuclear condensation, dysplasia of neurites in hippocampal pyramidal cells, thinning in pyramidal cell layer in hippocampus, and decrease in learning and memory of offspring mice.

High Temperature Induces Expression of Tobacco Transcription Factor NtMYC2a to Regulate Nicotine and JA Biosynthesis.

Environmental stress elevates the level of jasmonic acid (JA) and activates the biosynthesis of nicotine and related pyridine alkaloids in tobacco ( L.) by up-regulating the expression of putrescine -methyltransferase 1 (NtPMT1), which encodes a putrescine -methyl transferase that catalyzes nicotine formation. The JA signal suppressor JASMONATE ZIM DOMAIN 1 (NtJAZ1) and its target protein, NtMYC2a, also regulate nicotine biosynthesis; however, how these proteins interact to regulate abiotic-induced nicotine biosynthesis is poorly understood.

P31comet, a member of the synaptonemal complex, participates in meiotic DSB formation in rice.

The human mitotic arrest-deficient 2 (Mad2) binding protein p31(comet) participates in the spindle checkpoint and coordinates cell cycle events in mitosis although its function in meiosis remains unknown in all organisms. Here, we reveal P31(comet) as a synaptonemal complex (SC) protein in rice (Oryza sativa L.).

The Exonuclease Homolog OsRAD1 Promotes Accurate Meiotic Double-Strand Break Repair by Suppressing Nonhomologous End Joining.

During meiosis, programmed double-strand breaks (DSBs) are generated to initiate homologous recombination, which is crucial for faithful chromosome segregation. In yeast, Radiation sensitive1 (RAD1) acts together with Radiation sensitive9 (RAD9) and Hydroxyurea sensitive1 (HUS1) to facilitate meiotic recombination via cell-cycle checkpoint control. However, little is known about the meiotic functions of these proteins in higher eukaryotes.

Carbon Monoxide Interacts with Auxin and Nitric Oxide to Cope with Iron Deficiency in Arabidopsis.

To clarify the roles of carbon monoxide (CO), nitric oxide (NO), and auxin in the plant response to iron deficiency (-Fe), and to establish how the signaling molecules interact to enhance Fe acquisition, we conducted physiological, genetic, and molecular analyses that compared the responses of various Arabidopsis mutants, including hy1 (CO deficient), noa1 (NO deficient), nia1/nia2 (NO deficient), yuc1 (auxin over-accumulation), and cue1 (NO over-accumulation) to -Fe stress. We also generated a HY1 over-expression line (named HY1-OX) in which CO is over-produced compared to wild-type. We found that the suppression of CO and NO generation using various inhibitors enhanced the sensitivity of wild-type plants to Fe depletion.

The Dynamic Changes of the Plasma Membrane Proteins and the Protective Roles of Nitric Oxide in Rice Subjected to Heavy Metal Cadmium Stress.

The heavy metal cadmium is a common environmental contaminant in soils and has adverse effects on crop growth and development. The signaling processes in plants that initiate cellular responses to environmental stress have been shown to be located in the plasma membrane (PM). A better understanding of the PM proteome in response to environmental stress might provide new insights for improving stress-tolerant crops.

[Genome-wide analysis and functional prediction of the Trihelix transcription factor family in rice].

The Trihelix transcription factor family plays an essential role in plant growth, development and stress response. However, the studies about identification and analysis of this gene family in rice on the genome-wide level have not been reported. In this study, 31 members of the Trihelix family, which contain highly conserved and characteristic trihelix domain through sequence clustering and functional domains analysis, were identified in rice genome database using bioinformatic tools.

OsSDS is essential for DSB formation in rice meiosis.

SDS is a meiosis specific cyclin-like protein and required for DMC1 mediated double-strand break (DSB) repairing in Arabidopsis. Here, we found its rice homolog, OsSDS, is essential for meiotic DSB formation. The Ossds mutant is normal in vegetative growth but both male and female gametes are inviable.

MRE11 is required for homologous synapsis and DSB processing in rice meiosis.

Mre11, a conserved protein found in organisms ranging from yeast to multicellular organisms, is required for normal meiotic recombination. Mre11 interacts with Rad50 and Nbs1/Xrs2 to form a complex (MRN/X) that participates in double-strand break (DSB) ends processing. In this study, we silenced the MRE11 gene in rice and detailed its function using molecular and cytological methods.