scholarly journals A genetic framework for regulation and seasonal adaptation of shoot architecture in hybrid aspen

2020 ◽  
Vol 117 (21) ◽  
pp. 11523-11530 ◽  
Author(s):  
Jay P. Maurya ◽  
Pal C. Miskolczi ◽  
Sanatkumar Mishra ◽  
Rajesh Kumar Singh ◽  
Rishikesh P. Bhalerao
Keyword(s):  
Growth Control ◽  
Genetic Network ◽  
Dependent Manner ◽  
Hybrid Aspen ◽  
Seasonal Growth ◽  
Seasonal Adaptation ◽  
Antagonistic Action ◽  
Shoot Architecture ◽  
Terminal Flower 1 ◽  
Simultaneous Activation

Shoot architecture is critical for optimizing plant adaptation and productivity. In contrast with annuals, branching in perennials native to temperate and boreal regions must be coordinated with seasonal growth cycles. How branching is coordinated with seasonal growth is poorly understood. We identified key components of the genetic network that controls branching and its regulation by seasonal cues in the model tree hybrid aspen. Our results demonstrate that branching and its control by seasonal cues is mediated by mutually antagonistic action of aspen orthologs of the flowering regulatorsTERMINAL FLOWER 1(TFL1) andAPETALA1(LIKE APETALA 1/LAP1).LAP1promotes branching through local action in axillary buds.LAP1acts in a cytokinin-dependent manner, stimulating expression of the cell-cycle regulatorAIL1and suppressingBRANCHED1expression to promote branching. Short photoperiod and low temperature, the major seasonal cues heralding winter, suppress branching by simultaneous activation ofTFL1and repression of theLAP1pathway. Our results thus reveal the genetic network mediating control of branching and its regulation by environmental cues facilitating integration of branching with seasonal growth control in perennial trees.

scholarly journals Long-range mobile signals mediate seasonal control of shoot growth

2019 ◽  
Vol 116 (22) ◽  
pp. 10852-10857 ◽  
Author(s):  
Pál Miskolczi ◽  
Rajesh Kumar Singh ◽  
Szymon Tylewicz ◽  
Abdul Azeez ◽  
Jay P. Maurya ◽  
...  
Keyword(s):  
Shoot Apex ◽  
Shoot Growth ◽  
Plant Hormone ◽  
Growth Control ◽  
Growth Patterns ◽  
Seasonal Growth ◽  
Flowering Locus T ◽  
Adaptive Growth ◽  
Terminal Flower 1 ◽  
Systemic Signals

In perennial plants, seasonal shifts provide cues that control adaptive growth patterns of the shoot apex. However, where these seasonal cues are sensed and communicated to the shoot apex remains unknown. We demonstrate that systemic signals from leaves play key roles in seasonal control of shoot growth in model tree hybrid aspen. Grafting experiments reveal that the tree ortholog of Arabidopsis flowering time regulator FLOWERING LOCUS T (FT) and the plant hormone gibberellic acid (GA) systemically convey seasonal cues to the shoot apex. GA (unlike FT) also acts locally in shoot apex, downstream of FT in seasonal growth control. At the shoot apex, antagonistic factors—LAP1, a target of FT and the FT antagonist TERMINAL FLOWER 1 (TFL1)—act locally to promote and suppress seasonal growth, respectively. These data reveal seasonal changes perceived in leaves that are communicated to the shoot apex by systemic signals that, in concert with locally acting components, control adaptive growth patterns.

scholarly journals Potential transceptor AtNRT1.13 modulates shoot architecture and flowering time in a nitrate-dependent manner

2021 ◽  
Author(s):  
Hui-Yu Chen ◽  
Shan-Hua Lin ◽  
Ling-Hsin Cheng ◽  
Jeng-Jong Wu ◽  
Yi-Chen Lin ◽  
...  
Keyword(s):  
Flowering Time ◽  
Nitrate Transport ◽  
Dependent Manner ◽  
Transport Activity ◽  
Node Number ◽  
Shoot Architecture ◽  
Glucuronidase Reporter ◽  
Uptake Activity ◽  
Delayed Flowering ◽  
Severe Growth

Abstract Compared with root development regulated by external nutrients, less is known about how internal nutrients are monitored to control plasticity of shoot development. In this study, we characterize an Arabidopsis thaliana transceptor, NRT1.13 (NPF4.4), of the NRT1/PTR/NPF family. Different from most NRT1 transporters, NRT1.13 does not have the conserved proline residue between transmembrane domains 10 and 11; an essential residue for nitrate transport activity in CHL1/NRT1.1/NPF6.3. As expected, when expressed in oocytes, NRT1.13 showed no nitrate transport activity. However, when Ser 487 at the corresponding position was converted back to proline, NRT1.13 S487P regained nitrate uptake activity, suggesting that wild-type NRT1.13 cannot transport nitrate but can bind it. Subcellular localization and β-glucuronidase reporter analyses indicated that NRT1.13 is a plasma membrane protein expressed at the parenchyma cells next to xylem in the petioles and the stem nodes. When plants were grown with a normal concentration of nitrate, nrt1.13 showed no severe growth phenotype. However, when grown under low-nitrate conditions, nrt1.13 showed delayed flowering, increased node number, retarded branch outgrowth, and reduced lateral nitrate allocation to nodes. Our results suggest that NRT1.13 is required for low-nitrate acclimation and that internal nitrate is monitored near the xylem by NRT1.13 to regulate shoot architecture and flowering time.

Myostatin increases human trophoblast cell invasion by upregulating N-cadherin via SMAD2/3-SMAD4 Signaling

2022 ◽  
Author(s):  
Faten AbdelHafez Ahmed ◽  
Christian Klausen ◽  
Hua Zhu ◽  
Peter C K Leung
Keyword(s):  
Cell Invasion ◽  
Transforming Growth Factor ◽  
Muscle Growth ◽  
Growth Control ◽  
Trophoblast Cell ◽  
Type I ◽  
Dependent Manner ◽  
Placental Development ◽  
Human Trophoblast ◽  
Protein Levels

Abstract Placental insufficiency disorders are major obstetric complications that share a common phenomenon of poor placental trophoblast cell invasion and remodeling of uterine tissues. Myostatin is a transforming growth factor (TGF)-β superfamily member well-known for its important role in muscle growth control. Myostatin is also produced in the placenta and has been shown to regulate some trophoblast functions. However, its roles in placental development are still poorly understood. In this study, we tested the hypothesis that myostatin increases trophoblast cell invasion by upregulating N-cadherin via SMAD2/3-SMAD4 signaling. Primary and immortalized (HTR8/SVneo) trophoblast cells were used as study models. Matrigel-coated transwell invasion assays were used to study the effects of recombinant human myostatin on trophoblast cell invasion. RT-qPCR and Western blot were used to measure myostatin effects on N-cadherin mRNA and protein levels, respectively. Small inhibitor molecules as well as siRNA-mediated knockdown were used to block myostatin receptor and downstream signaling, respectively. Data were analyzed either by unpaired Student T test or one-way ANOVA followed by Newman Keuls test for multiple group comparisons. Myostatin significantly increased primary and HTR8/SVneo trophoblast cell invasion. Moreover, myostatin upregulated N-cadherin mRNA and protein levels in a time dependent manner in both study models. These effects were blocked by inhibition of TGF-β type I receptors as well as siRNA-mediated knockdown of SMAD2/3 combined or common SMAD4. Importantly, myostatin-induced trophoblast cell invasion was abolished by knockdown of N-cadherin, SMAD2/3 or SMAD4. Myostatin may increase human trophoblast cell invasion by upregulating N-cadherin via SMAD2/3-SMAD4 signaling.

scholarly journals Regulation of Cell Diameter, For3p Localization, and Cell Symmetry by Fission Yeast Rho-GAP Rga4p

2007 ◽  
Vol 18 (6) ◽  
pp. 2090-2101 ◽  
Author(s):  
Maitreyi Das ◽  
David J. Wiley ◽  
Saskia Medina ◽  
Helen A. Vincent ◽  
Michelle Larrea ◽  
...  
Keyword(s):  
Cell Growth ◽  
Growth Control ◽  
Cell Diameter ◽  
Dependent Manner ◽  
Cell Symmetry ◽  
Actin Cable ◽  
Growing Cell ◽  
Development And Differentiation ◽  
Negative Role ◽  
Cell Growth Control

Control of cellular dimensions and cell symmetry are critical for development and differentiation. Here we provide evidence that the putative Rho-GAP Rga4p of Schizosaccharomyces pombe controls cellular dimensions. rga4Δ cells are wider in diameter and shorter in length, whereas Rga4p overexpression leads to reduced diameter of the growing cell tip. Consistent with a negative role in cell growth control, Rga4p protein localizes to the cell sides in a “corset” pattern, and to the nongrowing cell tips. Additionally, rga4Δ cells show an altered growth pattern similar to that observed in mutants of the formin homology protein For3p. Consistent with these observations, Rga4p is required for normal localization of For3p and for normal distribution of the actin cytoskeleton. We show that different domains of the Rga4p protein mediate diverse morphological functions. The C-terminal GAP domain mediates For3p localization to the cell tips and maintains cell diameter. Conversely, overexpression of the N-terminal LIM homology domain of Rga4p promotes actin cable formation in a For3p-dependent manner. Our studies indicate that Rga4p functionally interacts with For3p and has a novel function in the control of cell diameter and cell growth.

scholarly journals A genetic network mediating the control of bud break in hybrid aspen

2018 ◽  
Vol 9 (1) ◽  
Author(s):  
Rajesh Kumar Singh ◽  
Jay P. Maurya ◽  
Abdul Azeez ◽  
Pal Miskolczi ◽  
Szymon Tylewicz ◽  
...  
Keyword(s):  
Genetic Network ◽  
Bud Break ◽  
Hybrid Aspen

scholarly journals The Traditional Japanese Medicine Rikkunshito Promotes Gastric Emptying via the Antagonistic Action of the 5-HT3Receptor Pathway in Rats

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
K. Tominaga ◽  
T. Kido ◽  
M. Ochi ◽  
C. Sadakane ◽  
A. Mase ◽  
...  
Keyword(s):  
Gastric Emptying ◽  
Receptor Agonist ◽  
Delayed Gastric Emptying ◽  
Maximum Effect ◽  
Phenol Red ◽  
Dependent Manner ◽  
Antagonistic Action ◽  
Traditional Japanese Medicine ◽  
Male Wistar Rats ◽  
Dose Dependent

The traditional Japanese medicine rikkunshito ameliorates the nitric oxide-associated delay in gastric emptying. Whether rikkunshito affects gastric motility associated with 5-hydroxytryptamine (serotonin: 5-HT) receptors or dopamine receptors is unknown. We examined the effects of rikkunshito on the delay in gastric emptying induced by 5-HT or dopamine using the phenol red method in male Wistar rats. 5-HT (0.01–1.0 mg kg−1, i.p.) dose dependently delayed gastric emptying, similar to the effect of the 5-HT3receptor agonist 1-(3-chlorophenyl) biguanide (0.01–1.0 mg kg−1, i.p.). Dopamine also dose dependently delayed gastric emptying. The 5-HT3receptor antagonist ondansetron (0.04–4.0 mg kg−1) and rikkunshito (125–500 mg kg−1) significantly suppressed the delay in gastric emptying caused by 5-HT or 1-(3-chlorophenyl) biguanide. Hesperidin (the most active ingredient in rikkunshito) suppressed the 5-HT-induced delayed gastric emptying in a dose-dependent manner, the maximum effect of which was similar to that of ondansetron (0.4 mg kg−1). The improvement obtained by rikkunshito or ondansetron in delaying gastric emptying was completely blocked by pretreatment with atropine. Rikkunshito appears to improve delay in gastric emptying via the antagonistic action of the 5-HT3receptor pathway.

scholarly journals Thyroid Hormone Action Is Disrupted by Bisphenol A as an Antagonist

2002 ◽  
Vol 87 (11) ◽  
pp. 5185-5190 ◽  
Author(s):  
Kenji Moriyama ◽  
Tetsuya Tagami ◽  
Takashi Akamizu ◽  
Takeshi Usui ◽  
Misa Saijo ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Bisphenol A ◽  
Hormone Receptors ◽  
Transient Gene Expression ◽  
Transcriptional Level ◽  
Dependent Manner ◽  
Inhibitory Effects ◽  
Antagonistic Action ◽  
Estrogenic Properties ◽  
Dose Dependent

Abstract Bisphenol A (BPA), a monomer of polycarbonate plastics, has been shown to possess estrogenic properties and act as an agonist for the estrogen receptors. Although an epidemiologically based investigation has suggested that some chemicals could disrupt thyroid function in animals, the effects on thyroid hormone receptors (TRs) are unknown. We show here that BPA inhibits TR-mediated transcription by acting as an antagonist. In the transient gene expression experiments, BPA suppressed transcriptional activity that is stimulated by thyroid hormone (T3) in a dose-dependent manner. The inhibitory effects were observed in the presence of physiological concentrations of T3. In contrast, in the case of negatively regulated TSHα promoter, BPA activated the gene transcription that is suppressed by T3. To elucidate possible mechanisms of the antagonistic action of BPA, the effects on T3 binding and cofactor interaction with TR were examined. The Ki value for BPA was 200 μm when assessed by inhibition of [125I]T3 binding to rat hepatic nuclear TRs. In a mammalian two-hybrid assay, BPA recruited the nuclear corepressor to the TR. These results suggest that BPA could displace T3 from the TR and recruit a transcriptional repressor, resulting in gene suppression. This is the first report that BPA can antagonize T3 action at the transcriptional level. BPA may disrupt the function of various types of nuclear hormone receptors and their cofactors to disturb our internal hormonal environment.

scholarly journals Neuropeptide Y reduces expression of social fear via simultaneous activation of Y1 and Y2 receptors

2019 ◽  
Vol 33 (12) ◽  
pp. 1533-1539 ◽  
Author(s):  
Johannes Kornhuber ◽  
Iulia Zoicas
Keyword(s):  
Neuropeptide Y ◽  
Receptor Antagonist ◽  
Social Experience ◽  
Fear Extinction ◽  
Dependent Manner ◽  
Contextual Fear ◽  
Y1 Receptor ◽  
Y2 Receptor ◽  
Social Fear ◽  
Simultaneous Activation

Background: Neuropeptide Y (NPY) has anxiolytic effects and facilitates extinction of cued and contextual fear in rodents, thereby acting as a resilience factor against exaggerated fear responses after adverse events. We investigated whether NPY influences acquisition, expression and extinction of social fear in a mouse model of social fear conditioning (SFC). Methods: NPY was administered intracerebroventricularly before SFC or before social fear extinction with or without prior administration of Y1 and/or Y2 receptor antagonists. Results: We show that NPY affects SFC-induced social fear in a time point–dependent manner. When administered before SFC, NPY did not affect acquisition, expression and extinction of social fear. However, when administered before social fear extinction, NPY reduced expression of social fear via simultaneous activation of Y1 and Y2 receptors. As such, neither the Y1 receptor antagonist BIBO3304 trifluoroacetate nor the Y2 receptor antagonist BIIE0246 was able to block the effects of NPY completely. However, when administered in combination, they completely blocked the effects of NPY on social fear expression. Conclusions: These findings have important clinical implications, as they suggest that although medication strategies aimed at increasing brain NPY activity are unlikely to prevent the formation of aversive memories after a traumatic social experience, they might improve the recovery from a traumatic social experience by reducing the expression of social fear.

scholarly journals Branching Regulator BRC1 Mediates Photoperiodic Control of Seasonal Growth in Hybrid Aspen

2020 ◽  
Vol 30 (1) ◽  
pp. 122-126.e2 ◽  
Author(s):  
Jay P. Maurya ◽  
Rajesh Kumar Singh ◽  
Pal C. Miskolczi ◽  
Amritha N. Prasad ◽  
Kristoffer Jonsson ◽  
...  
Keyword(s):  
Hybrid Aspen ◽  
Seasonal Growth ◽  
Photoperiodic Control

2-Chlorodeoxyadenosine (2-CDA) and Dexamethasone Induce Apoptosis in Multiple Myeloma (MM) Via Different Mechanisms.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4792-4792
Author(s):  
Bolin Liu ◽  
Zeying Fang ◽  
Jian Ma ◽  
Thomas E. Dillon ◽  
Tim E. Byers ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Growth Inhibition ◽  
Cell Lines ◽  
B Lymphocyte ◽  
Therapeutic Potential ◽  
Growth Control ◽  
Cross Resistance ◽  
Dependent Manner ◽  
Caspase 9 ◽  
Ic50 Values

Abstract Although 2-CDA has been active on B-lymphocyte derived malignancies, its potential for myeloma growth control has not been fully investigated. In the present study on a pair of MM cell lines, dexamethasone-sensitive (MM1.S) and dexamethasone-resistant (MM1.R), we sought to determine whether 2-CDA can effectively induce apoptosis and growth inhibition in both cell lines and whether there is cross resistance between 2-CDA and dexamethasone in MM1.R cells. Cell proliferation assay (MTS) releaved that 2-CDA significantly inhibited both MM1.S and MM1.R cell growth in a dose dependent manner, with the minimum (10%) and maximum (100%) inhibition concentration of 12.5 nM/L and 500 nM/L for the MM1.S, and 25 nM/L and 500 nM/L for the MM1.R cells, respectively. The IC50 values of 2-CDA in the MM1.S and MM1.R cells were 48 nM/L and 60 nM/L, respectively. No cross resistance was observed between 2-CDA and dexamethasone in the MM1.R cells. On the molecular level, dexamethasone induced PARP and caspase-9 cleavage, and increased the level of p27kip1 only in the MM1.S cells. 2-CDA treatment in both cell lines resulted in DNA fragmentation as well as strong PARP and caspase-9 cleavage, but no significant changes in the levels of P-Akt, P-MARK, p27kip1, E2F1, and cyclin D1, indicating that 2-CDA induces growth inhibition and cell death in MM cell lines likely through mitochondria-dependent apoptotic mechanism. Cell cycle analyses by flow cytometry showed that dexamethasone (5μM/L) treatment increased sub-G1 (apoptosis) cells to 8.1% only in the MM1.S cells, while the majority (87%) of cells were arrested in the G1 phase of cell cycle in 24 hours. In contrast, 2-CDA (0.5μM/L for 24 hours) strongly induced apoptosis in both cell lines (sub-G1 population increased to 19.6% and 22.1% for the MM1.S and MM1.R cells, respectively) without changing their cell cycle profiles. These data suggest that dexamethasone and 2-CDA induce apoptosis in myeloma cells via different mechanisms, which would provide a theoretical basis for combination therapy for MM with these two agents. Furthermore, our results also show that 2-CDA alone is capable of inducing apoptosis in the MM1.R cells, suggesting that 2-CDA may have therapeutic potential for MM patients with a dexamethasone-resistant phenotype.

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