scholarly journals Apple B-box factors regulate light-responsive anthocyanin biosynthesis genes

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Blue J. Plunkett ◽  
Rebecca Henry-Kirk ◽  
Adam Friend ◽  
Robert Diack ◽  
Susanne Helbig ◽  
...  
Keyword(s):  
Anthocyanin Biosynthesis ◽  
Dependent Manner ◽  
Fruit Colour ◽  
Temperature Dependent ◽  
Environmental Signals ◽  
Over Expression ◽  
Ethylene Content ◽  
Environmentally Responsive ◽  
Anthocyanin Biosynthetic Genes

AbstractEnvironmentally-responsive genes can affect fruit red colour via the activation of MYB transcription factors. The apple B-box (BBX) gene, BBX33/CONSTANS-like 11 (COL11) has been reported to influence apple red-skin colour in a light- and temperature-dependent manner. To further understand the role of apple BBX genes, other members of the BBX family were examined for effects on colour regulation. Expression of 23 BBX genes in apple skin was analysed during fruit development. We investigated the diurnal rhythm of expression of the BBX genes, the anthocyanin biosynthetic genes and a MYB activator, MYB10. Transactivation assays on the MYB10 promoter, showed that BBX proteins 1, 17, 15, 35, 51, and 54 were able to directly function as activators. Using truncated versions of the MYB10 promoter, a key region was identified for activation by BBX1. BBX1 enhanced the activation of MYB10 and MdbHLH3 on the promoter of the anthocyanin biosynthetic gene DFR. In transformed apple lines, over-expression of BBX1 reduced internal ethylene content and altered both cyanidin concentration and associated gene expression. We propose that, along with environmental signals, the control of MYB10 expression by BBXs in ‘Royal Gala’ fruit involves the integration of the expression of multiple BBXs to regulate fruit colour.

scholarly journals Time-dependent sequestration of RVE8 by LNK proteins shapes the diurnal oscillation of anthocyanin biosynthesis

2015 ◽  
Vol 112 (16) ◽  
pp. 5249-5253 ◽  
Author(s):  
Pablo Pérez-García ◽  
Yuan Ma ◽  
Marcelo J. Yanovsky ◽  
Paloma Mas
Keyword(s):  
Gene Expression ◽  
Chromatin Immunoprecipitation ◽  
Clock Genes ◽  
Anthocyanin Biosynthesis ◽  
Environmental Signals ◽  
The Past ◽  
Diurnal Oscillation ◽  
Target Promoters ◽  
Anthocyanin Biosynthetic Genes

Circadian clocks sustain 24-h rhythms in physiology and metabolism that are synchronized with the day/night cycle. In plants, the regulatory network responsible for the generation of rhythms has been broadly investigated over the past years. However, little is known about the intersecting pathways that link the environmental signals with rhythms in cellular metabolism. Here, we examine the role of the circadian components REVEILLE8/LHY-CCA1-LIKE5 (RVE8/LCL5) and NIGHT LIGHT–INDUCIBLE AND CLOCK-REGULATED genes (LNK) shaping the diurnal oscillation of the anthocyanin metabolic pathway. Around dawn, RVE8 up-regulates anthocyanin gene expression by directly associating to the promoters of a subset of anthocyanin biosynthetic genes. The up-regulation is overcome at midday by the repressing activity of LNK proteins, as inferred by the increased anthocyanin gene expression in lnk1/lnk2 double mutant plants. Chromatin immunoprecipitation assays using LNK and RVE8 misexpressing plants show that RVE8 binding to target promoters is precluded in LNK overexpressing plants and conversely, binding is enhanced in the absence of functional LNKs, which provides a mechanism by which LNKs antagonize RVE8 function in the regulation of anthocyanin accumulation. Based on their previously described transcriptional coactivating function, our study defines a switch in the regulatory activity of RVE8–LNK interaction, from a synergic coactivating role of evening-expressed clock genes to a repressive antagonistic function modulating anthocyanin biosynthesis around midday.

scholarly journals Loss of DIAPH3, a Formin Family Protein, Leads to Cytokinetic Failure Only under High Temperature Conditions in Mouse FM3A Cells

2020 ◽  
Vol 21 (22) ◽  
pp. 8493
Author(s):  
Hiroki Kazama ◽  
Shu-ichiro Kashiwaba ◽  
Sayaka Ishii ◽  
Keiko Yoshida ◽  
Yuta Yatsuo ◽  
...  
Keyword(s):  
Cell Division ◽  
High Temperature ◽  
Temperature Sensitive ◽  
Dependent Manner ◽  
Temperature Dependent ◽  
Over Expression ◽  
Temperature Conditions ◽  
Family Protein ◽  
Temperature Environment ◽  
Ts Mutant

Cell division is essential for the maintenance of life and involves chromosome segregation and subsequent cytokinesis. The processes are tightly regulated at both the spatial and temporal level by various genes, and failures in this regulation are associated with oncogenesis. Here, we investigated the gene responsible for defects in cell division by using murine temperature-sensitive (ts) mutant strains, tsFT101 and tsFT50 cells. The ts mutants normally grow in a low temperature environment (32 °C) but fail to divide in a high temperature environment (39 °C). Exome sequencing and over-expression analyses identified Diaph3, a member of the formin family, as the cause of the temperature sensitivity observed in tsFT101 and tsFT50 cells. Interestingly, Diaph3 knockout cells showed abnormality in cytokinesis at 39 °C, and the phenotype was rescued by re-expression of Diaph3 WT, but not Diaph1 and Diaph2, other members of the formin family. Furthermore, Diaph3 knockout cells cultured at 39 °C showed a significant increase in the level of acetylated α-tubulin, an index of stabilized microtubules, and the level was reduced by Diaph3 expression. These results suggest that Diaph3 is required for cytokinesis only under high temperature conditions. Therefore, our study provides a new insight into the mechanisms by which regulatory factors of cell division function in a temperature-dependent manner.

Antitumor Genotoxic Agents, Such as Fludarabine*, Doxorubincin or Cis-Platine, Induce Activation of STAT1 in a p53 Protein Dependent Manner.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4384-4384
Author(s):  
Ibtissam Youlyouz-Marfak ◽  
Christophe Le Clorennec ◽  
Imen Najjar ◽  
Fanny Baran-Marszak ◽  
Nathalie Gachard ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
P53 Protein ◽  
Surrogate Marker ◽  
Dependent Manner ◽  
Hl60 Cells ◽  
Over Expression ◽  
Cellular Models ◽  
Genotoxic Agents ◽  
P53 Activation

Abstract Introduction: Chemotherapeutic drug such as Fludarabine*; doxorubicin or cis-platine induce cell cycle arrest and apoptosis via activation of p53. Convergent studies suggest that p53 and STAT1 cooperate in the induction of apoptosis, and that STAT1 favors p53 activation. However, to our knowledge, the role of p53 in the activation of STAT1 is not documented. We present our results suggesting that (i) genotoxic agents are STAT1 inducers, (ii) STAT1 activation depends on the presence of p53 protein, and (iii) this phenomenon is modulated by the tyrosine kinase inhibitor STI571. Materials and Methods: To analyse the role of p53 in STAT1 activation, we have used different cellular models with different p53 status: PRI (p53wt), BL2 (p53wt), BL41 (p53 mutated on Arg248, resulting in the loss of p53 DNA binding activity (p53mut)), Jurkat, HL60 and MEF (the 3 latter being p53 null). The following cDNAs were used for functional studies: p53wt, p53mut, MDM2 and MTBP (MDM2 transforming protein). These cDNAs were cloned either in a pcDNA3 vector or a pRT-1 inducible vector (in the latter, the gene of interest is expressed from a bidirectional doxycycline regulatable promoter allowing simultaneous expression of truncated NGF receptor, used as a surrogate marker of inducibility). Results: Treatment of the different cell lines with the 3 genotoxic drugs Fludarabine*, doxorubicin or cis-platine induced STAT1 activation in p53wt BL2 or PRI cells and in p53mut BL41 cells, but not in Jurkat cells neither in HL60 or MEF cells. Induction of STAT1 was also obtained in presence of the RNA synthesis inhibitor Actinomycin D or in presence of secretion inhibitor Brefeldine A. Over-expression of p53wt or p53mut markedly increased STAT1 activation in PRI cells. This effect was reversed by over-expression of MTBP. Complementation of both HL60 and MEF cells with both p53wt and p53mut cDNA induced constitutive STAT1 activation, an effect that was increased by treatment with doxorubine in transfected HL60 cells. This effect was reversed by over-expression of MDM2 in HL60 cells. Finally, we found that treatment of cells with the inhibitor STI 571 of c-Abl tyrosine kinase, a kinase known to be associated with ATM during p53 activation, decreased STAT1 activation by genotoxic drugs. Conclusion: Our results show that genotoxic agents are inducers of STAT1, that p53 protein but not p53 transcriptional activity is responsible for this STAT1 activation, and suggest a possible involvement the cABL tyrosine kinase.

Brain O2 consumption and glutamate release during hypoglycemic coma in piglets are temperature sensitive

1999 ◽  
Vol 276 (6) ◽  
pp. H2053-H2062 ◽  
Author(s):  
R. N. Ichord ◽  
F. J. Northington ◽  
D. van Wylen ◽  
M. V. Johnston ◽  
C. Kwon ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Brain Temperature ◽  
Glutamate Release ◽  
Temperature Sensitive ◽  
Dependent Manner ◽  
Temperature Dependent ◽  
Immature Brain ◽  
Hypoglycemic Coma ◽  
Mature Brain

Hypoglycemic injury in the mature brain is mediated by excitotoxicity, which is worsened by disordered cellular energy metabolism. The role of excitotoxicity in relation to brain energy metabolism during hypoglycemia has not been studied in the immature brain. Brain oxygen consumption ([Formula: see text]) increases during hypoglycemia in piglets, whereas [Formula: see text] decreases in adult pig models. We tested the hypothesis that increased[Formula: see text] during hypoglycemic coma is temperature dependent and coincides with increased excitatory amino acids (EAA). We measured cerebral blood flow (CBF),[Formula: see text], and cortical microdiaysate EAA in pentobarbital-anesthetized piglets during hypoglycemic coma and during 2 h of recovery and in normoglycemic controls. In warmed animals brain temperature was kept normothermic (38.5°C). In unwarmed animals brain temperature was allowed to fall (37.6°C). During hypoglycemia CBF increased similarly in warmed animals and unwarmed animals;[Formula: see text] increased in warmed animals but not unwarmed animals. Glutamate increased during coma and increased more in warmed animals than unwarmed animals but normalized quickly during recovery. EEG recovered earlier in unwarmed animals. We conclude that during a hypoglycemic coma in the immature brain,[Formula: see text] and glutamate are increased in a temperature-dependent manner.

scholarly journals Role of AT1G72910, AT1G72940, and ADR1-LIKE 2 in Plant Immunity under Nonsense-Mediated mRNA Decay-Compromised Conditions at Low Temperatures

2020 ◽  
Vol 21 (21) ◽  
pp. 7986
Author(s):  
Zeeshan Nasim ◽  
Muhammad Fahim ◽  
Katarzyna Gawarecka ◽  
Hendry Susila ◽  
Suhyun Jin ◽  
...  
Keyword(s):  
Pseudomonas Syringae ◽  
Mrna Decay ◽  
Degradation Kinetics ◽  
Plant Immunity ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Temperature Dependent ◽  
Stunted Growth ◽  
Nonsense Mediated Mrna Decay

Nonsense-mediated mRNA decay (NMD) removes aberrant transcripts to avoid the accumulation of truncated proteins. NMD regulates nucleotide-binding, leucine-rich repeat (NLR) genes to prevent autoimmunity; however, the function of a large number of NLRs still remains poorly understood. Here, we show that three NLR genes (AT1G72910, AT1G72940, and ADR1-LIKE 2) are important for NMD-mediated regulation of defense signaling at lower temperatures. At 16 °C, the NMD-compromised up-frameshift protein1 (upf1) upf3 mutants showed growth arrest that can be rescued by the artificial miRNA-mediated knockdown of the three NLR genes. mRNA levels of these NLRs are induced by Pseudomonas syringae inoculation and exogenous SA treatment. Mutations in AT1G72910, AT1G72940, and ADR1-LIKE 2 genes resulted in increased susceptibility to Pseudomonas syringae, whereas their overexpression resulted in severely stunted growth, which was dependent on basal disease resistance genes. The NMD-deficient upf1 upf3 mutants accumulated higher levels of NMD signature-containing transcripts from these NLR genes at 16 °C. Furthermore, mRNA degradation kinetics showed that these NMD signature-containing transcripts were more stable in upf1 upf3 mutants. Based on these findings, we propose that AT1G72910, AT1G72940, and ADR1-LIKE 2 are directly regulated by NMD in a temperature-dependent manner and play an important role in modulating plant immunity at lower temperatures.

scholarly journals Epigenetic modification associated with climate regulates betulin biosynthesis in birch

2021 ◽  
Author(s):  
Jiang Wang ◽  
Bowei Chen ◽  
Shahid Ali ◽  
Tianxu Zhang ◽  
Yu Wang ◽  
...  
Keyword(s):  
Climate Change ◽  
Dna Methylation ◽  
Climatic Factors ◽  
Epigenetic Modification ◽  
Summer Precipitation ◽  
Dependent Manner ◽  
White Birch ◽  
Environmental Signals ◽  
Pentacyclic Triterpenoid

AbstractThe Betula genus contains pentacyclic triterpenoid betulin known for its environmental adaptation and medicinal properties. However, the mechanisms underlying betulin biosynthesis responding to climate change remain unclear. In this study, the role of epigenetic modification (DNA methylation) in betulin biosynthesis was examined and how climatic factors influence it. Whole-genome bisulfite sequencing was performed for greenhouse-grown Chinese white birch (Betula platyphylla Sukaczev) treated with DNA methylation inhibitor zebularine (ZEB) and a natural birch population in Northeast China. ZEB treatment significantly affected the CHH methylation level of transposable elements and betulin content in a hormesis dose-dependent manner. The methylation and expression of bHLH9, a key transcriptional factor controlling betulin biosynthesis, were also consistently affected by ZEB treatment as a hormetic dose–response. In the natural population, there was a positive correlation between promoter methylation of bHLH9 and summer precipitation, while winter temperature was negatively correlated. Thus climate-dependent methylation of bHLH9 regulates the expression of downstream genes involved in betulin biosynthesis. This study highlights the role of environmental signals to induce epigenetic changes that result in betulin production, possibly helping to develop resilient plants to combat ongoing climate change and enhance secondary metabolite production.

scholarly journals Overexpression of TCP8 delays Arabidopsis flowering through a FLOWERING LOCUS C-dependent pathway

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Xiaoyan Wang ◽  
Xintong Xu ◽  
Xiaowei Mo ◽  
Luyao Zhong ◽  
Jiancong Zhang ◽  
...  
Keyword(s):  
Mrna Level ◽  
Dependent Manner ◽  
Loss Of Function ◽  
Flowering Locus C ◽  
Environmental Signals ◽  
Growth Defects ◽  
Flowering Control ◽  
Flowering Locus ◽  
Delayed Flowering

Abstract Background Flowering is a key process in the life cycle of plants. The transition from vegetative to reproductive growth is thus under sophisticated regulation by endogenous and environmental signals. The plant-specific Teosinte Branched 1/Cycloidea/Proliferating Cell Factors (TCP) family transcription factors are involved in many biological processes, but their roles in regulating flowering have not been totally elucidated. Results We explored the role of Arabidopsis TCP8 in plant development and, especially, in flowering control. Overexpression of TCP8 significantly delayed flowering under both long-day and short-day conditions and dominant repression by TCP8 led to various growth defects. The upregulation of TCP8 led to more accumulated mRNA level of FLOWERING LOCUS C (FLC), a central floral repressor of Arabidopsis. TCP8 functions in an FLC-dependent manner, as TCP8 overexpression in the flc-6 loss-of-function mutant failed to delay flowering. The vernalization treatment could reverse the late flowering phenotype caused by TCP8 overexpression. Conclusions Our results provide evidence for a role of TCP8 in flowering control and add to our knowledge of the molecular basis of TCP8 function.

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