A systemic increase in the recombination frequency upon local infection of Arabidopsis thaliana plants with oilseed rape mosaic virus depends on plant age, the initial inoculum concentration and the time for virus replication

Sherpa Romeo green journal: open accessIn the past, we showed that loca linfection of tobacco leaves with either tobacco mosaic virus or oilseed rape mosaic virus (ORMV) resulted in a systemic increase in the homologous recombination frequency (HRF). Later on, we showed that a similar phenomenon occurs in Arabidopsis thaliana plant sinfected with ORMV. Here, we tested whether the time of removing the infected leaves as well as viral titer have any effect on the degree of changes in HRF in systemic tissues. An increase in HRF in systemic non-infected tissues was more pronounced when the infected leaves were detached from the infected plants at 60–96 h post-infection, rather than at earlier time. Next, we found that exposure to higher concentrations of inoculum was much more efficient in triggering an increase in HRF than exposure to lower concentrations. Finally, we showed that older plants exhibited a higher increase in HRF than younger plants. We found that an increase in genome instability in systemic tissues of locally infected plants depends on plant age, the concentration of initial in oculums and the time of viral replication.Ye

Transgenerational changes in the genome stability and methylation in pathogen-infected plants: (Virus-induced plant genome instability)

Previously, we reported the generation of a virus-induced systemic signal that increased the somatic and meiotic recombination rates in tobacco mosaic virus (TMV)-infected tobacco plants. Here, we analyzed the progeny of plants that received the signal and found that these plants also have a higher frequency of rearrangements in the loci carrying the homology to LRR region of the gene of resistance to TMV (N-gene). Analysis of the stability of repetitive elements from Nicotiana tabacum loci and 5.8S ribosomal RNA loci did not show any changes. Further analysis of the changes in the progeny of infected plants revealed that they had substantially hypermethylated genomes. At the same time, loci-specific methylation analysis showed: (1) profound hypomethylation in several LRR-containing loci; (2) substantial hypermethylation of actin loci and (3) no change in methylation in the loci of repetitive elements from N. tabacum or 5.8S ribosomal RNA. Global genome hypermethylation of the progeny is believed to be part of a general protection mechanism against stress, whereas locus-specific hypomethylation is associated with a higher frequency of rearrangements. Increased recombination events combined with the specific methylation pattern induced by pathogen attack could be a sign of an adaptive response by plants

X-ray spectral correlations in a sample of Low-mass black hole X-ray binaries in the hard state

The power-law emission and reflection component provide valuable insights into the accretion process around a black hole. In this work, thanks to the broadband spectra coverage of \emph{the Nuclear Spectroscopic Telescope Array}, we study the spectral properties for a sample of low-mass black hole X-ray binaries (BHXRBs). We find that there is a positive correlation between the photon index $\Gamma$ and the reflection fraction $R$ (the ratio of the coronal intensity that illuminates the disk to the coronal intensity that reaches the observer), consistent with previous studies, but except for MAXI J1820+070. It is quite interesting that this source also deviates from the well-known ``V"-shaped correlation between the photon index $\Gamma$ and the X-ray luminosity log$L_{\rm X}$, when it is in the bright hard state. More specifically, the $\Lambda$-shaped correlation between $\Gamma$ and log$L_{\rm X}$ is observed, as the luminosity decreases by a factor of 3 in a narrow range from $\sim 10^{38}$ to $10^{37.5}$ $\rm erg~s^{-1}$. Furthermore, we discover a strong positive correlation between $R$ and the X-ray luminosity for BHXRBs in the hard state, which puts a constraint on the disk-corona coupling and the evolution.Comment: 18 pages, 9 figures, 3 tables, Accepted for publication in Ap

Transgenerational Adaptation of Arabidopsis to Stress Requires DNA Methylation and the Function of Dicer-Like Proteins

Epigenetic states and certain environmental responses in mammals and seed plants can persist in the next sexual generation. These transgenerational effects have potential adaptative significance as well as medical and agronomic ramifications. Recent evidence suggests that some abiotic and biotic stress responses of plants are transgenerational. For example, viral infection of tobacco plants and exposure of Arabidopsis thaliana plants to UVC and flagellin can induce transgenerational increases in homologous recombination frequency (HRF). Here we show that exposure of Arabidopsis plants to stresses, including salt, UVC, cold, heat and flood, resulted in a higher HRF, increased global genome methylation, and higher tolerance to stress in the untreated progeny. This transgenerational effect did not, however, persist in successive generations. Treatment of the progeny of stressed plants with 5-azacytidine was shown to decrease global genomic methylation and enhance stress tolerance. Dicer-like (DCL) 2 and DCL3 encode Dicer activities important for small RNA-dependent gene silencing. Stress-induced HRF and DNA methylation were impaired in dcl2 and dcl3 deficiency mutants, while in dcl2 mutants, only stress-induced stress tolerance was impaired. Our results are consistent with the hypothesis that stress-induced transgenerational responses in Arabidopsis depend on altered DNA methylation and smRNA silencing pathways

Elevated atmospheric CO2 concentration triggers redistribution of nitrogen to promote tillering in rice

Elevated atmospheric CO2 concentration (eCO2) often reduces nitrogen (N) content in rice plants and stimulates tillering. However, there is a general consensus that reduced N would constrain rice tillering. To resolve this contradiction, we investigated N distribution and transcriptomic changes in different rice plant organs after subjecting them to eCO2 and different N application rates. Our results showed that eCO2 significantly promoted rice tillers (by 0.6, 1.1, 1.7, and 2.1 tillers/plant at 0, 75, 150, and 225 kg N ha−1 N application rates, respectively) and more tillers were produced under higher N application rates, confirming that N availability constrained tillering in the early stages of growth. Although N content declined in the leaves (−11.0 to −20.7 mg g−1) and sheaths (−9.8 to −28.8 mg g−1) of rice plants exposed to eCO2, the N content of newly emerged tillers on plants exposed to eCO2 equaled or exceeded the N content of tillers produced under ambient CO2 conditions. Apparently, the redistribution of N within the plant per se was a critical adaptation strategy to the eCO2 condition. Transcriptomic analysis revealed that eCO2 induced less extensive alteration of gene expression than did N application. Most importantly, the expression levels of multiple N-related transporters and receptors such as nitrate transporter NRT2.3a/b and NRT1.1a/b were differentially regulated in leaf and shoot apical meristem, suggesting that multiple genes were involved in sensing the N signal and transporting N metabolites to adapt to eCO2. The redistribution of N in different organs could be a universal adaptation strategy of terrestrial plants to eCO2

Lifetime stress cumulatively programs brain transcriptome and impedes stroke recovery: benefit of sensory stimulation

Sherpa Romeo green journal, open accessPrenatal stress (PS) represents a critical variable affecting lifetime health trajectories, metabolic and vascular functions. Beneficial experiences may attenuate the effects of PS and its programming of health outcomes in later life. Here we investigated in a rat model (1) if PS modulates recovery following cortical ischemia in adulthood; (2) if a second hit by adult stress (AS) exaggerates stress responses and ischemic damage; and (3) if tactile stimulation (TS) attenuates the cumulative effects of PS and AS. Prenatally stressed and non-stressed adult male rats underwent focal ischemic motor cortex lesion and were tested in skilled reaching and skilled walking tasks. Two groups of rats experienced recurrent restraint stress in adulthood and one of these groups also underwent daily TS therapy. Animals that experienced both PS and AS displayed the most severe motor disabilities after lesion. By contrast, TS promoted recovery from ischemic lesion and reduced hypothalamic-pituitary-adrenal axis activity. The data also showed that cumulative effects of adverse and beneficial lifespan experiences interact with disease outcomes and brain plasticity through the modulation of gene expression. Microarray analysis of the lesion motor cortex revealed that cumulative PS and AS interact with genes related to growth factors and transcription factors, which were not affected by PS or lesion alone. TS in PS+AS animals reverted these changes, suggesting a critical role for these factors in activity-dependent motor cortical reorganization after ischemic lesion. These findings suggest that beneficial experience later in life can moderate adverse consequences of early programming to improve cerebrovascular health.Ye

Maternal stress induces eipgenetic signatures of psychiatric and neurological diseases in the offspring

Sherpa Romeo green journal: open accessThe gestational state is a period of particular vulnerability to diseases that affect maternal and fetal health. Stress during gestation may represent a powerful influence on maternal mental health and offspring brain plasticity and development. Here we show that the fetal transcriptome, through microRNA (miRNA) regulation, responds to prenatal stress in association with epigenetic signatures of psychiatric and neurological diseases. Pregnant Long-Evans rats were assigned to stress from gestational days 12 to 18 while others served as handled controls. Gestational stress in the dam disrupted parturient maternal behaviour and was accompanied by characteristic brain miRNA profiles in the mother and her offspring, and altered transcriptomic brain profiles in the offspring. In the offspring brains, prenatal stress upregulated miR-103, which is involved in brain pathologies, and downregulated its potential gene target Ptplb. Prenatal stress downregulated miR-145, a marker of multiple sclerosis in humans. Prenatal stress also upregulated miR-323 and miR-98, which may alter inflammatory responses in the brain. Furthermore, prenatal stress upregulated miR-219, which targets the gene Dazap1. Both miR-219 and Dazap1 are putative markers of schizophrenia and bipolar affective disorder in humans. Offspring transcriptomic changes included genes related to development, axonal guidance and neuropathology. These findings indicate that prenatal stress modifies epigenetic signatures linked to disease during critical periods of fetal brain development. These observations provide a new mechanistic association between environmental and genetic risk factors in psychiatric and neurological disease.Ye

Ancestral exposure to stress epigenetically programs preterm birth risk and adverse maternal and newborn outcomes

Sherpa Romeo green journal: open accessAbstract Background: Chronic stress is considered to be one of many causes of human preterm birth (PTB), but no direct evidence has yet been provided. Here we show in rats that stress across generations has downstream effects on endocrine, metabolic and behavioural manifestations of PTB possibly via microRNA (miRNA) regulation. Methods: Pregnant dams of the parental generation were exposed to stress from gestational days 12 to 18. Their pregnant daughters (F1) and grand-daughters (F2) either were stressed or remained as non-stressed controls. Gestational length, maternal gestational weight gain, blood glucose and plasma corticosterone levels, litter size and offspring weight gain from postnatal days 1 to 30 were recorded in each generation, including F3. Maternal behaviours were analysed for the first hour after completed parturition, and offspring sensorimotor development was recorded on postnatal day (P) 7. F0 through F2 maternal brain frontal cortex, uterus and placenta miRNA and gene expression patterns were used to identify stress-induced epigenetic regulatory pathways of maternal behaviour and pregnancy maintenance. Results: Progressively up to the F2 generation, stress gradually reduced gestational length, maternal weight gain and behavioural activity, and increased blood glucose levels. Reduced offspring growth and delayed behavioural development in the stress cohort was recognizable as early as P7, with the greatest effect in the F3 offspring of transgenerationally stressed mothers. Furthermore, stress altered miRNA expression patterns in the brain and uterus of F2 mothers, including the miR-200 family, which regulates pathways related to brain plasticity and parturition, respectively. Main miR-200 family target genes in the uterus, Stat5b, Zeb1 and Zeb2, were downregulated by multigenerational stress in the F1 generation. Zeb2 was also reduced in the stressed F2 generation, suggesting a causal mechanism for disturbed pregnancy maintenance. Additionally, stress increased placental miR-181a, a marker of human PTB. Conclusions: The findings indicate that a family history of stress may program central and peripheral pathways regulating gestational length and maternal and newborn health outcomes in the maternal lineage. This new paradigm may model the origin of many human PTB causes.Ye