scholarly journals ABA represses TOR and root meristem activity through nuclear exit of the SnRK1 kinase

2021 ◽  
Author(s):  
Borja Belda-Palazon ◽  
Monica Costa ◽  
Tom Beeckman ◽  
Filip Rolland ◽  
Elena Baena-Gonzalez
Keyword(s):  
Cell Proliferation ◽  
Nuclear Export ◽  
Growth Regulation ◽  
Root Meristem ◽  
Plant Tolerance ◽  
Proliferation Zone ◽  
Meristem Size ◽  
Main Driver ◽  
Root Meristematic Cells ◽  
Underlying Mechanisms

The phytohormone abscisic acid (ABA) promotes plant tolerance to major stresses like drought, partly by modulating plant growth and development. However, the underlying mechanisms are poorly understood. Here, we show that cell proliferation in the Arabidopsis thaliana root meristem is controlled by the interplay between three kinases, SNF1-RELATED KINASE 2 (SnRK2), the main driver of ABA signaling, the SnRK1 energy sensor, and the growth-promoting TARGET OF RAPAMYCIN (TOR) kinase. Under favorable conditions, the SnRK1α1 catalytic subunit is enriched in the nuclei of root meristematic cells and this is accompanied by normal cell proliferation and meristem size. Depletion of SnRK2s in a snrk2.2 snrk2.3 double mutant causes constitutive cytoplasmic localization of SnRK1α1 and a reduction in meristem size, suggesting that, under non-stress conditions, SnRK2s enable growth by retaining SnRK1α1 in the nucleus. In response to elevated ABA levels, SnRK1α1 translocates to the cytoplasm and this is accompanied by inhibition of TOR, decreased cell proliferation and meristem size. Blocking nuclear export with leptomycin B abrogates ABA-driven SnRK1α1 relocalization to the cytoplasm and the inhibition of TOR. Fusion of SnRK1α1 to an SV40 nuclear localization signal leads to defective TOR repression in response to ABA, demonstrating that SnRK1α1 nuclear exit is a premise for this repression. Finally, the SnRK2-dependent changes in SnRK1α1 subcellular localization are specific to the proliferation zone of the meristem, underscoring the relevance of this mechanism for growth regulation.

scholarly journals Spatial differences in stoichiometry of EGR phosphatase and Microtubule-Associated Stress Protein 1 control root meristem activity during drought stress.

2021 ◽  
Author(s):  
Toshisagba Longkumer ◽  
Chih-Yun Chen ◽  
Marco Biancucci ◽  
Bhaskara Govinal Badiger ◽  
Paul E. Verslues
Keyword(s):  
Cell Division ◽  
Cell Size ◽  
Cell Expansion ◽  
Growth Regulation ◽  
Root Meristem ◽  
Stress Protein ◽  
Root Cell ◽  
Root Cortex ◽  
Meristem Cell ◽  
Meristem Size

During moderate severity drought and low water potential (Ψw) stress, poorly understood signaling mechanisms restrict both meristem cell division and subsequent cell expansion. We found that the Clade E Growth-Regulating 2 (EGR2) protein phosphatase and Microtubule Associated Stress Protein 1 (MASP1) differed in their stoichiometry of expression across the root meristem and had opposing effects on root meristem activity at low Ψw. Ectopic MASP1 or EGR expression increased or decreased, respectively, root meristem size and root elongation during low Ψw stress. This, along with the ability of phosphomimic MASP1 to overcome EGR suppression of root meristem size and observation that ectopic EGR expression had no effect on unstressed plants, indicated that during low Ψw EGR activation and attenuation of MASP1 phosphorylation in their overlapping zone of expression determines root meristem size and activity. Ectopic EGR expression also decreased root cell size at low Ψw. Conversely, both the egr1-1egr2-1 and egr1-1egr2-1masp1-1 mutants had similarly increased root cell size; but, only egr1-1egr2-1 had increased cell division. These observations demonstrated that EGRs affect meristem activity via MASP1 but affect cell expansion via other mechanisms. Interestingly, EGR2 was highly expressed in the root cortex, a cell type important for growth regulation and environmental response.

scholarly journals Supraoptimal Brassinosteroid Levels Inhibit Root Growth by Reducing Root Meristem and Cell Elongation in Rice

Plants ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1962
Author(s):  
Kewalee Jantapo ◽  
Watcharapong Wimonchaijit ◽  
Wenfei Wang ◽  
Juthamas Chaiwanon
Keyword(s):  
Cell Proliferation ◽  
Root Growth ◽  
Cell Elongation ◽  
Root Meristem ◽  
Oryza Sativa L ◽  
Rice Root ◽  
Meristem Size ◽  
A Genome ◽  
Meristem Development ◽  
N Deficiency

Root growth depends on cell proliferation and cell elongation at the root meristem, which are controlled by plant hormones and nutrient availability. As a foraging strategy, rice (Oryza sativa L.) grows longer roots when nitrogen (N) is scarce. However, how the plant steroid hormone brassinosteroid (BR) regulates rice root meristem development and responses to N deficiency remains unclear. Here, we show that BR has a negative effect on meristem size and a dose-dependent effect on cell elongation in roots of rice seedlings treated with exogenous BR (24-epicastasterone, ECS) and the BR biosynthesis inhibitor propiconazole (PPZ). A genome-wide transcriptome analysis identified 4110 and 3076 differentially expressed genes in response to ECS and PPZ treatments, respectively. The gene ontology (GO) analysis shows that terms related to cell proliferation and cell elongation were enriched among the ECS-repressed genes. Furthermore, microscopic analysis of ECS- and PPZ-treated roots grown under N-sufficient and N-deficient conditions demonstrates that exogenous BR or PPZ application could not enhance N deficiency-mediated root elongation promotion as the treatments could not promote root meristem size and cell elongation simultaneously. Our study demonstrates that optimal levels of BR in the rice root meristem are crucial for optimal root growth and the foraging response to N deficiency.

scholarly journals From Micro to Long: Non-Coding RNAs in Tamoxifen Resistance of Breast Cancer Cells

Cancers ◽  
2021 ◽  
Vol 13 (15) ◽  
pp. 3688
Author(s):  
Jéssica Fernanda Barazetti ◽  
Tayana Shultz Jucoski ◽  
Tamyres Mingorance Carvalho ◽  
Rafaela Nasser Veiga ◽  
Ana Flávia Kohler ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Hormone Receptor ◽  
Estrogen Receptor Alpha ◽  
Expression Patterns ◽  
Tamoxifen Resistance ◽  
Hormone Receptor Positive ◽  
Current State ◽  
Main Driver ◽  
Underlying Mechanisms ◽  
Multiple Signaling

Breast cancer is the most commonly diagnosed cancer and the leading cause of cancer mortality among women. Two thirds of patients are classified as hormone receptor positive, based on expression of estrogen receptor alpha (ERα), the main driver of breast cancer cell proliferation, and/or progesterone receptor, which is regulated by ERα. Despite presenting the best prognosis, these tumors can recur when patients acquire resistance to treatment by aromatase inhibitors or antiestrogen such as tamoxifen (Tam). The mechanisms that are involved in Tam resistance are complex and involve multiple signaling pathways. Recently, roles for microRNAs and lncRNAs in controlling ER expression and/or tamoxifen action have been described, but the underlying mechanisms are still little explored. In this review, we will discuss the current state of knowledge on the roles of microRNAs and lncRNAs in the main mechanisms of tamoxifen resistance in hormone receptor positive breast cancer. In the future, this knowledge can be used to identify patients at a greater risk of relapse due to the expression patterns of ncRNAs that impact response to Tam, in order to guide their treatment more efficiently and possibly to design therapeutic strategies to bypass mechanisms of resistance.

scholarly journals MiR-489-3p inhibits cell proliferation, migration, and invasion, and induces apoptosis, by targeting the BDNF-mediated PI3K/AKT pathway in glioblastoma

2020 ◽  
Vol 15 (1) ◽  
pp. 274-283
Author(s):  
Bo Zheng ◽  
Tao Chen
Keyword(s):  
Cell Proliferation ◽  
Luciferase Reporter ◽  
Akt Pathway ◽  
Migration And Invasion ◽  
Bdnf Mrna ◽  
Protein Levels ◽  
Rna Immunoprecipitation ◽  
Underlying Mechanisms ◽  
Induced Apoptosis ◽  
Protein Cell

AbstractAmong astrocyte tumors, glioblastoma (GBM) is the most malignant glioma, highly aggressive and invasive, with extremely poor prognosis. Previous research has reported that microRNAs (miRNAs) participate in the progression of many cancers. Thus, this study aimed to explore the role and the underlying mechanisms of microRNA (miR)-489-3p in GBM progression. The expression of miR-489-3p and brain-derived neurotrophic factor (BDNF) mRNA was measured by quantitative real-time polymerase chain reaction. Western blot analysis was used to detect BDNF protein and the PI3K/AKT pathway-related protein. Cell proliferation, apoptosis, migration, and invasion were analyzed using CKK-8 assay, flow cytometry, and transwell assay, respectively. The interaction between BDNF and miR-489-3p was explored by luciferase reporter assay and RNA immunoprecipitation (RIP) assay. MiR-489-3p was down-regulated and BDNF was up-regulated in GBM tissues and cells. MiR-489-3p re-expression or BDNF knockdown inhibited GBM cell proliferation, migration, and invasion, and promoted apoptosis. BDNF was a target of miR-489-3p, and BDNF up-regulation reversed the effects of miR-489-3p on GBM cells. The protein levels of p-AKT and p-PI3K were notably reduced in GBM cells by overexpression of miR-489-3p, but were rescued following BDNF up-regulation. Therefore, miR-489-3p inhibited proliferation, migration, and invasion, and induced apoptosis, by targeting the BDNF-mediated PI3K/AKT pathway in GBM, providing new strategies for clinical treatment of GBM.

scholarly journals Sirtuin 1 and Sirtuin 3 in Granulosa Cell Tumors

2021 ◽  
Vol 22 (4) ◽  
pp. 2047
Author(s):  
Nina Schmid ◽  
Kim-Gwendolyn Dietrich ◽  
Ignasi Forne ◽  
Alexander Burges ◽  
Magdalena Szymanska ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Granulosa Cell ◽  
Granulosa Cells ◽  
Drug Targets ◽  
Growth Regulation ◽  
Sirtuin 1 ◽  
Ki 67 ◽  
Granulosa Cell Tumors ◽  
Novel Drug

Sirtuins (SIRTs) are NAD+-dependent deacetylases that regulate proliferation and cell death. In the human ovary, granulosa cells express sirtuin 1 (SIRT1), which has also been detected in human tumors derived from granulosa cells, i.e., granulosa cell tumors (GCTs), and in KGN cells. KGN cells are an established cellular model for the majority of GCTs and were used to explore the role of SIRT1. The SIRT1 activator SRT2104 increased cell proliferation. By contrast, the inhibitor EX527 reduced cell numbers, without inducing apoptosis. These results were supported by the outcome of siRNA-mediated silencing studies. A tissue microarray containing 92 GCTs revealed nuclear and/or cytoplasmic SIRT1 staining in the majority of the samples, and also, SIRT2-7 were detected in most samples. The expression of SIRT1–7 was not correlated with the survival of the patients; however, SIRT3 and SIRT7 expression was significantly correlated with the proliferation marker Ki-67, implying roles in tumor cell proliferation. SIRT3 was identified by a proteomic analysis as the most abundant SIRT in KGN. The results of the siRNA-silencing experiments indicate involvement of SIRT3 in proliferation. Thus, several SIRTs are expressed by GCTs, and SIRT1 and SIRT3 are involved in the growth regulation of KGN. If transferable to GCTs, these SIRTs may represent novel drug targets.

scholarly journals A potential feedback loop underlying glacial-interglacial cycles

2021 ◽  
Author(s):  
Els Weinans ◽  
Anne Willem Omta ◽  
George A. K. van Voorn ◽  
Egbert H. van Nes
Keyword(s):  
Ocean Circulation ◽  
Feedback Loop ◽  
Atmospheric Temperature ◽  
Earth System ◽  
Biological Productivity ◽  
Ocean Ventilation ◽  
The Earth ◽  
Main Driver ◽  
Underlying Mechanisms ◽  
Convergent Cross Mapping

AbstractThe sawtooth-patterned glacial-interglacial cycles in the Earth’s atmospheric temperature are a well-known, though poorly understood phenomenon. Pinpointing the relevant mechanisms behind these cycles will not only provide insights into past climate dynamics, but also help predict possible future responses of the Earth system to changing CO$$_2$$ 2 levels. Previous work on this phenomenon suggests that the most important underlying mechanisms are interactions between marine biological production, ocean circulation, temperature and dust. So far, interaction directions (i.e., what causes what) have remained elusive. In this paper, we apply Convergent Cross-Mapping (CCM) to analyze paleoclimatic and paleoceanographic records to elucidate which mechanisms proposed in the literature play an important role in glacial-interglacial cycles, and to test the directionality of interactions. We find causal links between ocean ventilation, biological productivity, benthic $$\delta ^{18}$$ δ 18 O and dust, consistent with some but not all of the mechanisms proposed in the literature. Most importantly, we find evidence for a potential feedback loop from ocean ventilation to biological productivity to climate back to ocean ventilation. Here, we propose the hypothesis that this feedback loop of connected mechanisms could be the main driver for the glacial-interglacial cycles.

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