scholarly journals Comparative Transcriptomics of Tropical Woody Plants Supports Fast and Furious Strategy along the Leaf Economics Spectrum in Lianas.

2021 ◽  
Author(s):  
Uğur Uzay Sezen ◽  
Samantha J. Worthy ◽  
Maria N. Umaña ◽  
Stuart J. Davies ◽  
Sean M McMahon ◽  
...  
Keyword(s):  
Woody Plants ◽  
Cell Cycle Progression ◽  
Genetic Basis ◽  
Shade Avoidance ◽  
Cycle Progression ◽  
Leaf Economics Spectrum ◽  
Tropical Plant ◽  
Tropical Woody Plants ◽  
And Function ◽  
Leaf Economics

Lianas, climbing woody plants, influence the structure and function of tropical forests. Climbing traits have evolved multiple times, including ancestral groups such as gymnosperms and pteridophytes, but the genetic basis of the liana strategy is largely unknown. Here, we use a comparative transcriptomic approach for 47 tropical plant species, including ten lianas of diverse taxonomic origins, to identify genes that are consistently expressed or downregulated only in lianas. Our comparative analysis of full-length transcripts enabled the identification of a core interactomic network common to lianas. Sets of transcripts identified from our analysis reveal features related to functional traits pertinent to leaf economics spectrum in lianas, include upregulation of genes controlling epidermal cuticular properties, cell wall remodeling, carbon concentrating mechanism, cell cycle progression, DNA repair and a large suit of downregulated transcription factors and enzymes involved in ABA-mediated stress response as well as lignin and suberin synthesis. All together, these genes are known to be significant in shaping plant morphologies through responses such as gravitropism, phyllotaxy and shade avoidance.

scholarly journals LINC00963 affects the development of colorectal cancer via MiR-532-3p/HMGA2 axis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jinjun Ye ◽  
Jidong Liu ◽  
Tao Tang ◽  
Le Xin ◽  
Xing Bao ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Growth ◽  
Cell Cycle Progression ◽  
Bioinformatics Analysis ◽  
Scratch Test ◽  
Luciferase Assay ◽  
Migration And Invasion ◽  
Cycle Progression ◽  
Ki67 Expression ◽  
And Function

Abstract Background LINC00963 is high-expressed in various carcinomas, but its expression and function in colorectal cancer (CRC) have not been explored. This study explored the role and mechanism of LINC00963 in CRC. Methods The expression of LINC00963 in CRC and its relationship with prognosis were examined by starBase and survival analysis. The effects of LINC00963, miR-532-3p and HMGA2 on the biological characteristics and EMT-related genes of CRC cells were studied by RT-qPCR, CCK-8, clone formation experiments, flow cytometry, scratch test, Transwell, and Western blot. Xenograft assay and immunohistochemistry were performed to verify the effect of LINC00963 on tumor growth. The correlation among LINC00963, miR-532-3p, and HMGA2 was analyzed by bioinformatics analysis, luciferase assay, and Pearson test. Results LINC00963 was high-expressed in CRC, and this was associated with poor prognosis of CRC. Silencing LINC00963 inhibited the activity, proliferation, migration, and invasion of CRC cells, MMP-3 and MMP-9 expressions, moreover, it also blocked cell cycle progression, and inhibited tumor growth and Ki67 expression. However, overexpression of LINC00963 showed the opposite effects to silencing LINC00963. LINC00963 targeted miR-532-3p to regulate HMGA2 expression. Down-regulation of miR-532-3p promoted cell proliferation, migration and invasion, and expressions of MMP-3 and MMP-9, and knockdown of HMGA2 reversed the effect of miR-532-3p inhibitor. Up-regulation of miR-532-3p inhibited the biological functions of CRC cells, and overexpression of HMGA2 reversed the miR-532-3p mimic effect. Conclusion LINC00963 affects the development of CRC through the miR-532-3p/HMGA2 axis.

Pentose Phosphate Pathway in Disease and Therapy

2014 ◽  
Vol 995 ◽  
pp. 1-27 ◽  
Author(s):  
Mahbuba Rahman ◽  
M. Rubayet Hasan
Keyword(s):  
Metabolic Pathways ◽  
Cell Cycle Progression ◽  
Metabolic Diseases ◽  
Pentose Phosphate ◽  
Cycle Progression ◽  
Novel Drugs ◽  
Abnormal Cells ◽  
Living Organisms ◽  
And Function

Pentose phosphate (PP) pathway, which is ubiquitously present in all living organisms, is one of the major metabolic pathways associated with glucose metabolism. The most important functions of this pathway includes the generation of reducing equivalents in the form of NADPH for reductive biosynthesis, and production of ribose sugars for the biosynthesis of nucleotides, amino acids, and other macromolecules required by all living cells. Under normal conditions of growth, PP pathway is important for cell cycle progression, myelin formation, and the maintenance of the structure and function of brain, liver, cortex and other organs. Under diseased conditions, such as in cases of many metabolic, neurological or malignant diseases, pathological mechanisms augment due to defects in the PP pathway genes. Adoption of alternative metabolic pathways by cells that are metabolically abnormal, or malignant cells that are resistant to chemotherapeutic drugs often plays important roles in disease progression and severity. Accordingly, the PP pathway has been suggested to play critical roles in protecting cancer or abnormal cells by providing reduced environment, to protect cells from oxidative damage and generating structural components for nucleic acids biosynthesis. Novel drugs that targets one or more components of the PP pathway could potentially serve to overcome challenges associated with currently available therapeutic options for many metabolic and non-metabolic diseases. However, careful designing of drugs is critical that takes into the accounts of cell’s broader genomic, proteomic and metabolic contexts under consideration, in order to avoid undesirable side-effects. In this review, we discuss the role of PP pathway under normal and abnormal physiological conditions and the potential of the PP pathway as a target for new drug development to treat metabolic and non-metabolic diseases.

scholarly journals Distinct Cell Cycle Timing Requirements for Extracellular Signal-Regulated Kinase and Phosphoinositide 3-Kinase Signaling Pathways in Somatic Cell Mitosis

2002 ◽  
Vol 22 (20) ◽  
pp. 7226-7241 ◽  
Author(s):  
Elisabeth C. Roberts ◽  
Paul S. Shapiro ◽  
Theresa Stines Nahreini ◽  
Gilles Pages ◽  
Jacques Pouyssegur ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Cyclin B1 ◽  
Erk Pathway ◽  
Cycle Progression ◽  
Mitotic Entry ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Phosphoinositide 3 Kinase ◽  
And Function

ABSTRACT Mitogen-activated protein (MAP) kinase and phosphoinositide 3-kinase (PI3K) pathways are necessary for cell cycle progression into S phase; however the importance of these pathways after the restriction point is poorly understood. In this study, we examined the regulation and function of extracellular signal-regulated kinase (ERK) and PI3K during G2/M in synchronized HeLa and NIH 3T3 cells. Phosphorylation and activation of both the MAP kinase kinase/ERK and PI3K/Akt pathways occur in late S and persist until the end of mitosis. Signaling was rapidly reversed by cell-permeable inhibitors, indicating that both pathways are continuously activated and rapidly cycle between active and inactive states during G2/M. The serum-dependent behavior of PI3K/Akt versus ERK pathway activation indicates that their mechanisms of regulation differ during G2/M. Effects of cell-permeable inhibitors and dominant-negative mutants show that both pathways are needed for mitotic progression. However, inhibiting the PI3K pathway interferes with cdc2 activation, cyclin B1 expression, and mitotic entry, whereas inhibiting the ERK pathway interferes with mitotic entry but has little effect on cdc2 activation and cyclin B1 and retards progression from metaphase to anaphase. Thus, our study provides novel evidence that ERK and PI3K pathways both promote cell cycle progression during G2/M but have different regulatory mechanisms and function at distinct times.

scholarly journals Tyr198 is the Essential Autophosphorylation Site for STK16 Localization and Kinase Activity

2019 ◽  
Vol 20 (19) ◽  
pp. 4852 ◽  
Author(s):  
Junjun Wang ◽  
Juanjuan Liu ◽  
Xinmiao Ji ◽  
Xin Zhang
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Kinase Activity ◽  
Kinase Domain ◽  
Serine Threonine Kinase ◽  
Cycle Progression ◽  
Threonine Kinase ◽  
Cellular Processes ◽  
Activation Segment ◽  
And Function

STK16, reported as a Golgi localized serine/threonine kinase, has been shown to participate in multiple cellular processes, including the TGF-β signaling pathway, TGN protein secretion and sorting, as well as cell cycle and Golgi assembly regulation. However, the mechanisms of the regulation of its kinase activity remain underexplored. It was known that STK16 is autophosphorylated at Thr185, Ser197, and Tyr198 of the activation segment in its kinase domain. We found that STK16 localizes to the cell membrane and the Golgi throughout the cell cycle, but mutations in the auto-phosphorylation sites not only alter its subcellular localization but also affect its kinase activity. In particular, the Tyr198 mutation alone significantly reduced the kinase activity of STK16, abolished its Golgi and membrane localization, and affected the cell cycle progression. This study demonstrates that a single site autophosphorylation of STK16 could affect its localization and function, which provides insights into the molecular regulatory mechanism of STK16’s kinase activity.

scholarly journals Building the right centriole for each cell type

2017 ◽  
Vol 217 (3) ◽  
pp. 823-835 ◽  
Author(s):  
Jadranka Loncarek ◽  
Mónica Bettencourt-Dias
Keyword(s):  
Cell Cycle Progression ◽  
Cell Types ◽  
Cell Type ◽  
Cycle Progression ◽  
Single Organism ◽  
Evolutionarily Conserved ◽  
The Right ◽  
And Function ◽  
The 19Th Century ◽  
High Resolution Microscopy

The centriole is a multifunctional structure that organizes centrosomes and cilia and is important for cell signaling, cell cycle progression, polarity, and motility. Defects in centriole number and structure are associated with human diseases including cancer and ciliopathies. Discovery of the centriole dates back to the 19th century. However, recent advances in genetic and biochemical tools, development of high-resolution microscopy, and identification of centriole components have accelerated our understanding of its assembly, function, evolution, and its role in human disease. The centriole is an evolutionarily conserved structure built from highly conserved proteins and is present in all branches of the eukaryotic tree of life. However, centriole number, size, and organization varies among different organisms and even cell types within a single organism, reflecting its cell type–specialized functions. In this review, we provide an overview of our current understanding of centriole biogenesis and how variations around the same theme generate alternatives for centriole formation and function.

scholarly journals Mammalian kinetochores count attached microtubules in a sensitive and switch-like manner to control cell cycle progression

2018 ◽  
Author(s):  
Jonathan Kuhn ◽  
Sophie Dumont
Keyword(s):  
Cell Cycle Progression ◽  
Spindle Assembly Checkpoint ◽  
Control Cell ◽  
Cycle Progression ◽  
Microtubule Binding ◽  
Input Signals ◽  
Pulling Forces ◽  
And Function ◽  
Robust Response ◽  
Control Cell Cycle Progression

AbstractThe Spindle Assembly Checkpoint (SAC) maintains genomic integrity by preventing anaphase until all kinetochores attach to the spindle. What specific signals are required for SAC satisfaction at mammalian kinetochores, and in what magnitude, are not well understood and central to understanding SAC signal processing and function. Here, we directly and independently tune candidate input signals – spindle forces and Hec1-microtubule binding – and map SAC outputs. By detaching microtubules from the spindle, we first demonstrate that the SAC does not respond to changes in spindle pulling forces. We then tune and fix the fraction of Hec1 molecules capable of microtubule binding, and interpret SAC output changes as coming from changes in binding, and not spindle forces. While the speed of satisfaction reduces with fewer attached microtubules, the kinetochore turns off the SAC even with few – approximately four – such microtubules. Thus, the mammalian kinetochore responds specifically to microtubule binding, and does so as a single, switch-like, sensitive unit. This may allow the kinetochore to rapidly react to attachments and maintain a robust response despite dynamic microtubule numbers.

scholarly journals The Golgi Protein GM130 Regulates Centrosome Morphology and Function

2008 ◽  
Vol 19 (2) ◽  
pp. 745-753 ◽  
Author(s):  
Andrew Kodani ◽  
Christine Sütterlin
Keyword(s):  
Mammalian Cells ◽  
Cell Cycle Progression ◽  
Human Cell Lines ◽  
Microtubule Organizing Center ◽  
Microtubule Organization ◽  
Cycle Progression ◽  
Multipolar Spindles ◽  
Organizing Center ◽  
Golgi Protein ◽  
And Function

The Golgi apparatus (GA) of mammalian cells is positioned in the vicinity of the centrosome, the major microtubule organizing center of the cell. The significance of this physical proximity for organelle function and cell cycle progression is only beginning to being understood. We have identified a novel function for the GA protein, GM130, in the regulation of centrosome morphology, position and function during interphase. RNA interference–mediated depletion of GM130 from five human cell lines revealed abnormal interphase centrosomes that were mispositioned and defective with respect to microtubule organization and cell migration. When GM130-depleted cells entered mitosis, they formed multipolar spindles, arrested in metaphase, and died. We also detected aberrant centrosomes during interphase and multipolar spindles during mitosis in ldlG cells, which do not contain detectable GM130. Although GA proteins have been described to regulate mitotic centrosomes and spindle formation, this is the first report of a role for a GA protein in the regulation of centrosomes during interphase.

Structure and function of the human parvulins Pin1 and Par14/17

2018 ◽  
Vol 399 (2) ◽  
pp. 101-125 ◽  
Author(s):  
Anja Matena ◽  
Edisa Rehic ◽  
Dana Hönig ◽  
Bianca Kamba ◽  
Peter Bayer
Keyword(s):  
Cell Fate ◽  
Metabolic Pathways ◽  
Ribosome Biogenesis ◽  
Cell Cycle Progression ◽  
Current Knowledge ◽  
Cycle Progression ◽  
Cell Fate Decisions ◽  
The Family ◽  
Broad Variety ◽  
And Function

AbstractParvulins belong to the family of peptidyl-prolylcis/transisomerases (PPIases) assisting in protein folding and in regulating the function of a broad variety of proteins in all branches of life. The human representatives Pin1 and Par14/17 are directly involved in processes influencing cellular maintenance and cell fate decisions such as cell-cycle progression, metabolic pathways and ribosome biogenesis. This review on human parvulins summarizes the current knowledge of these enzymes and intends to oppose the well-studied Pin1 to its less well-examined homolog human Par14/17 with respect to structure, catalytic and cellular function.

scholarly journals Dual control exerted by dopamine in blood-progenitor cell cycle regulation in Drosophila

2021 ◽  
Author(s):  
Tina Mukherjee ◽  
Ankita Kapoor ◽  
A Padmavathi
Keyword(s):  
Cell Cycle ◽  
Progenitor Cells ◽  
Progenitor Cell ◽  
Cell Cycle Progression ◽  
Lymph Gland ◽  
Cycle Progression ◽  
Myeloid Progenitor ◽  
G2 Phase ◽  
And Function ◽  
Cycle Regulation

In Drosophila, definitive hematopoiesis occurs in a specialized organ termed "lymph gland", where multi-potent stem-like blood progenitor cells reside and their homeostasis is central to growth of this organ. Recent findings have implicated a reliance on neurotransmitters in progenitor development and function however, our understanding of these molecules is still limited. Here, we extend our analysis and show that blood-progenitors are self-sufficient in synthesizing dopamine, a well-established neurotransmitter and have modules for its sensing through receptor and uptake via, transporter. Modulating their expression in progenitor cells affects lymph gland growth. Progenitor cell cycle analysis revealed an unexpected requirement for intracellular dopamine in progression of early progenitors from S to G2 phase of the cell cycle, while activation of dopamine-receptor later in development regulated the progression from G2 to entry into mitosis. The dual capacity in which dopamine operates, both intra-cellularly and extra-cellularly, controls lymph gland growth. These data highlight a novel and non-canonical use of dopamine as a proliferative cue by the myeloid-progenitor system and reveals a functional requirement for intracellular dopamine in cell-cycle progression.

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