scholarly journals Mechanism of Allium Crops Bulb Enlargement in Response to Photoperiod: A Review

2020 ◽  
Vol 21 (4) ◽  
pp. 1325 ◽  
Author(s):  
Muhammad Jawaad Atif ◽  
Mohammad Abass Ahanger ◽  
Bakht Amin ◽  
Muhammad Imran Ghani ◽  
Muhammad Ali ◽  
...  
Keyword(s):  
Present Review ◽  
Flowering Locus T ◽  
Allium Species ◽  
Significant Development ◽  
New Class ◽  
Bulb Formation ◽  
Signaling Mechanisms ◽  
Photoperiodic Regulation ◽  
Underlying Mechanisms ◽  
Practical Level

The photoperiod marks a varied set of behaviors in plants, including bulbing. Bulbing is controlled by inner signals, which can be stimulated or subdued by the ecological environment. It had been broadly stated that phytohormones control the plant development, and they are considered to play a significant part in the bulb formation. The past decade has witnessed significant progress in understanding and advancement about the photoperiodic initiation of bulbing in plants. A noticeable query is to what degree the mechanisms discovered in bulb crops are also shared by other species and what other qualities are also dependent on photoperiod. The FLOWERING LOCUS T (FT) protein has a role in flowering; however, the FT genes were afterward reported to play further functions in other biological developments (e.g., bulbing). This is predominantly applicable in photoperiodic regulation, where the FT genes seem to have experienced significant development at the practical level and play a novel part in the switch of bulb formation in Alliums. The neofunctionalization of FT homologs in the photoperiodic environments detects these proteins as a new class of primary signaling mechanisms that control the growth and organogenesis in these agronomic-related species. In the present review, we report the underlying mechanisms regulating the photoperiodic-mediated bulb enlargement in Allium species. Therefore, the present review aims to systematically review the published literature on the bulbing mechanism of Allium crops in response to photoperiod. We also provide evidence showing that the bulbing transitions are controlled by phytohormones signaling and FT-like paralogues that respond to independent environmental cues (photoperiod), and we also show that an autorelay mechanism involving FT modulates the expression of the bulbing-control gene. Although a large number of studies have been conducted, several limitations and research gaps have been identified that need to be addressed in future studies.

scholarly journals Temporal and Spatial Expression of Arabidopsis Gene Homologs Control Daylength Adaptation and Bulb Formation in Onion (Allium cepa L.)

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Md. Harun Ar Rashid ◽  
Wei Cheng ◽  
Brian Thomas
Keyword(s):  
Genetic Regulation ◽  
Specific Expression ◽  
Tissue Specific ◽  
Tissue Specific Expression ◽  
Bulb Formation ◽  
Photoperiodic Regulation ◽  
Allium Cepa L ◽  
New Varieties ◽  
Large Genome Size ◽  
High Level

Abstract Genetic studies aimed at onion improvement have been limited because of high heterozygosity, a very large genome size with a high level of repetitive DNA and a biennial life cycle. Onion bulb initiation is daylength-dependent, which places a significant barrier to adapting new varieties for growth at different latitudes. Compared to the photoperiodic regulation of flowering, relatively little is known about genetic regulation of the bulbing process. This study aims to identify the role of gene sequences involved in daylength-regulated bulb formation and tissue specific expression of onion. A comprehensive set of developmental and spatial quantitative mRNA expression experiments were carried out to investigate expression of onion FLOWERING LOCUS T (AcFT), LEAFY (AcLFY) and GIBBERELLIN-3 OXIDASE (GA3ox1) during the bulbing response. Bulbing ratios were used to measure the response of onion plants under long day (LD) and short day (SD) conditions. AcFT1 was expressed in LD, which induces bulb formation, while AcFT4 was expressed in SD, which inhibits bulb formation. AcFT5 and AcFT6 were expressed in LD and might also be involved in bulb formation itself. All AcFT, AcLFY and GA3ox1 genes showed distinctive patterns of tissue specific expression in onion, with AcFT genes found primarily in the sites of perception in the leaf and LFY in the basal tissues, the site of response. The results are consistent with AcFT1 expression being the signal for LD-induced bulb initiation and AcFT4, being involved in suppressing bulbing in SD.

scholarly journals Corrosion, Erosion and Wear Behavior of Complex Concentrated Alloys: A Review

Metals ◽  
2018 ◽  
Vol 8 (8) ◽  
pp. 603 ◽  
Author(s):  
Aditya Ayyagari ◽  
Vahid Hasannaeimi ◽  
Harpreet Grewal ◽  
Harpreet Arora ◽  
Sundeep Mukherjee
Keyword(s):  
Wear Behavior ◽  
Material Design ◽  
Degradation Mechanisms ◽  
New Paradigm ◽  
Alloy Development ◽  
Surface Degradation ◽  
High Entropy ◽  
New Class ◽  
Critical Knowledge ◽  
Underlying Mechanisms

There has been tremendous interest in recent years in a new class of multi-component metallic alloys that are referred to as high entropy alloys, or more generally, as complex concentrated alloys. These multi-principal element alloys represent a new paradigm in structural material design, where numerous desirable attributes are achieved simultaneously from multiple elements in equimolar (or near equimolar) proportions. While there are several review articles on alloy development, microstructure, mechanical behavior, and other bulk properties of these alloys, then there is a pressing need for an overview that is focused on their surface properties and surface degradation mechanisms. In this paper, we present a comprehensive view on corrosion, erosion and wear behavior of complex concentrated alloys. The effect of alloying elements, microstructure, and processing methods on the surface degradation behavior are analyzed and discussed in detail. We identify critical knowledge gaps in individual reports and highlight the underlying mechanisms and synergy between the different degradation routes.

Cracking novel shared targets between epilepsy and Alzheimer’s disease: need of the hour

2018 ◽  
Vol 29 (4) ◽  
pp. 425-442 ◽  
Author(s):  
Nitika Garg ◽  
Rupa Joshi ◽  
Bikash Medhi
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Vital Role ◽  
Present Review ◽  
The Common ◽  
Underlying Mechanisms ◽  
Gsk 3Β ◽  
Selection Of

Abstract Epilepsy and Alzheimer’s disease (AD) are interconnected. It is well known that seizures are linked with cognitive impairment, and there are various shared etiologies between epilepsy and AD. The connection between hyperexcitability of neurons and cognitive dysfunction in the progression of AD or epileptogenesis plays a vital role for improving selection of treatment for both diseases. Traditionally, seizures occur less frequently and in later stages of age in patients with AD which in turn implies that neurodegeneration causes seizures. The role of seizures in early stages of pathogenesis of AD is still an issue to be resolved. So, it is well timed to analyze the common pathways involved in pathophysiology of AD and epilepsy. The present review focuses on similar potential underlying mechanisms which may be related to the causes of seizures in epilepsy and cognitive impairment in AD. The proposed review will focus on many possible newer targets like abnormal expression of various enzymes like GSK-3β, PP2A, PKC, tau hyperphosphorylation, MMPs, caspases, neuroinflammation and oxidative stress associated with number of neurodegenerative diseases linked with epilepsy. The brief about the prospective line of treatment of both diseases will also be discussed in the present review.

Insights into LRRK2 function and dysfunction from transgenic and knockout rodent models

2012 ◽  
Vol 40 (5) ◽  
pp. 1080-1085 ◽  
Author(s):  
Maximilian Sloan ◽  
Javier Alegre-Abarrategui ◽  
Richard Wade-Martins
Keyword(s):  
Autosomal Dominant ◽  
Therapeutic Interventions ◽  
Present Review ◽  
Chromosome 12 ◽  
Rodent Models ◽  
Leucine Rich Repeat ◽  
Transgenic Expression ◽  
Cellular Processes ◽  
Cytoskeletal Dynamics ◽  
Underlying Mechanisms

Mutations in the LRRK2 (leucine-rich repeat kinase 2) gene on chromosome 12 cause autosomal dominant PD (Parkinson's disease), which is indistinguishable from sporadic forms of the disease. Numerous attempts have therefore been made to model PD in rodents via the transgenic expression of LRRK2 and its mutant variants and to elucidate the function of LRRK2 by knocking out rodent Lrrk2. Although these models often only partially recapitulate PD pathology, they have helped to elucidate both the normal and pathological function of LRRK2. In particular, LRRK2 has been suggested to play roles in cytoskeletal dynamics, synaptic machinery, dopamine homoeostasis and autophagic processes. Our understanding of how these pathways are affected, their contribution towards PD development and their interaction with one another is still incomplete, however. The present review summarizes the findings from LRRK2 rodent models and draws potential connections between the apparently disparate cellular processes altered, in order to better understand the underlying mechanisms of LRRK2 dysfunction and illuminate future therapeutic interventions.

JAK2-mediated intracellular signaling

2020 ◽  
Vol 20 ◽  
Author(s):  
Mentor Sopjani ◽  
Rifat Morina ◽  
Valdet Uka ◽  
Nguyen Thi Xuan ◽  
Miribane Dërmaku-Sopjani
Keyword(s):  
Receptor Tyrosine Kinase ◽  
Intracellular Signaling ◽  
Current Knowledge ◽  
Janus Kinase ◽  
Mediating Effects ◽  
Signaling Mechanisms ◽  
Recent Advances ◽  
Underlying Mechanisms ◽  
In The Beginning ◽  
Molecular Regulatory Mechanisms

: Janus kinase-2 (JAK2) is a non-receptor tyrosine kinase that serves key roles as the intracellular signaling effector of the cytokine receptor, such as mediating effects of leptin, erythropoietin, interferon, and growth hormone. A lot of molecular underlying mechanisms of JAK2 participation are known, however, additional signaling mechanisms of its activation, regulation, and pleiotropic signaling roles are still being explored. Here, we review the current knowledge of JAK2- mediated cellular signaling at the molecular level. In the beginning, we will focus on the recent advances in JAK2 activation and regulation. A part of our review focuses on the JAK2 involvement in various diseases/conditions. Recent advances highlight the molecular regulatory mechanisms utilized by the JAK2 signaling, thus, enabling to consider alternative therapeutic strategies to treat various diseases/conditions mediated by JAK2 by using it as a therapeutic target.

The bitter taste receptor (TAS2R) agonists denatonium and chloroquine display distinct patterns of relaxation of the guinea pig trachea

2012 ◽  
Vol 303 (11) ◽  
pp. L956-L966 ◽  
Author(s):  
Ville Pulkkinen ◽  
Martijn L. Manson ◽  
Jesper Säfholm ◽  
Mikael Adner ◽  
Sven-Erik Dahlén
Keyword(s):  
Guinea Pig ◽  
Bitter Taste ◽  
Taste Receptor ◽  
Prostaglandin E ◽  
Bitter Taste Receptor ◽  
New Class ◽  
Thromboxane Receptor ◽  
Signaling Mechanisms ◽  
Substantial Inhibition ◽  
Airway Physiology

Activation of taste receptors (TAS2Rs) by bitter taste agonists has been reported to cause bronchodilation. The aim of this study was to extend the information on the effects of bitter taste agonists on responses induced by different contractile mediators in a standard airway physiology preparation. Isometric responses were assessed in guinea pig trachea (GPT). TAS2R agonists were administered either to segments precontracted with different agonists for contraction or given before challenge with the different contractile stimuli, including antigen in tissues from ovalbumin-sensitized animals. TAS2R mRNA expression on GPT epithelium and smooth muscle was measured with real-time PCR. Denatonium, chloroquine, thiamine, and noscapine induced concentration-dependent relaxations (Rmax: 98.3 ± 1.6, 100.0 ± 0.0, 100.0 ± 0.0, and 52.3 ± 1.1% of maximum, respectively, in the presence of indomethacin) in segments precontracted with carbachol. The receptors for denatonium (TAS2R4, TAS2R10) and chloroquine (TAS2R3, TAS2R10) were expressed in GPT. Whereas denatonium selectively inhibited contractions induced by carbachol, chloroquine uniformly inhibited contractions evoked by prostaglandin E2, the thromboxane receptor agonist U-46619, leukotriene D4, histamine, and antigen. The effects of denatonium, but not those of chloroquine, were partly inhibited by blockers of the large Ca2+-activated K+ channels and decreased by an increase of the level of precontraction. In conclusion, TAS2R agonists mediated strong relaxations and substantial inhibition of contractions in GPT. Chloroquine and denatonium had distinct patterns of activity, indicating different signaling mechanisms. The findings reinforce the hypothesis that TAS2Rs are potential targets for the development of a new class of more efficacious agonists for bronchodilation.

scholarly journals The Role of Maresins in Inflammatory Pain: Function of Macrophages in Wound Regeneration

2019 ◽  
Vol 20 (23) ◽  
pp. 5849 ◽  
Author(s):  
Sung-Min Hwang ◽  
Gehoon Chung ◽  
Yong Ho Kim ◽  
Chul-Kyu Park
Keyword(s):  
Inflammatory Pain ◽  
Inflammatory Responses ◽  
M2 Macrophage ◽  
Macrophage Phenotype ◽  
New Class ◽  
Inflammatory Conditions ◽  
Signaling Mechanisms ◽  
Macrophage Phagocytosis ◽  
Anti Inflammatory

Although acute inflammatory responses are host-protective and generally self-limited, unresolved and delayed resolution of acute inflammation can lead to further tissue damage and chronic inflammation. The mechanism of pain induction under inflammatory conditions has been studied extensively; however, the mechanism of pain resolution is not fully understood. The resolution of inflammation is a biosynthetically active process, involving specialized pro-resolving mediators (SPMs). In particular, maresins (MaRs) are synthesized from docosahexaenoic acid (DHA) by macrophages and have anti-inflammatory and pro-resolving capacities as well as tissue regenerating and pain-relieving properties. A new class of macrophage-derived molecules—MaR conjugates in tissue regeneration (MCTRs)—has been reported to regulate phagocytosis and the repair and regeneration of damaged tissue. Macrophages not only participate in the biosynthesis of SPMs, but also play an important role in phagocytosis. They exhibit different phenotypes categorized as proinflammatory M1-like phenotypes and anti-inflammatory M2 phenotypes that mediate both harmful and protective functions, respectively. However, the signaling mechanisms underlying macrophage functions and phenotypic changes have not yet been fully established. Recent studies report that MaRs help resolve inflammatory pain by enhancing macrophage phagocytosis and shifting cytokine release to the anti-inflammatory M2 phenotypes. Consequently, this review elucidated the characteristics of MaRs and macrophages, focusing on the potent action of MaRs to enhance the M2 macrophage phenotype profiles that possess the ability to alleviate inflammatory pain.

scholarly journals A comparative perspective on lung and gill regeneration

2020 ◽  
Vol 223 (19) ◽  
pp. jeb226076
Author(s):  
Laura Cadiz ◽  
Michael G. Jonz
Keyword(s):  
Model Organisms ◽  
Comparative Approach ◽  
The Past ◽  
Tissue Replacement ◽  
Signaling Mechanisms ◽  
Aquatic Vertebrates ◽  
Mammalian Lung ◽  
The Common ◽  
Underlying Mechanisms ◽  
Lung Regeneration

ABSTRACTThe ability to continuously grow and regenerate the gills throughout life is a remarkable property of fish and amphibians. Considering that gill regeneration was first described over one century ago, it is surprising that the underlying mechanisms of cell and tissue replacement in the gills remain poorly understood. By contrast, the mammalian lung is a largely quiescent organ in adults but is capable of facultative regeneration following injury. In the course of the past decade, it has been recognized that lungs contain a population of stem or progenitor cells with an extensive ability to restore tissue; however, despite recent advances in regenerative biology of the lung, the signaling pathways that underlie regeneration are poorly understood. In this Review, we discuss the common evolutionary and embryological origins shared by gills and mammalian lungs. These are evident in homologies in tissue structure, cell populations, cellular function and genetic pathways. An integration of the literature on gill and lung regeneration in vertebrates is presented using a comparative approach in order to outline the challenges that remain in these areas, and to highlight the importance of using aquatic vertebrates as model organisms. The study of gill regeneration in fish and amphibians, which have a high regenerative potential and for which genetic tools are widely available, represents a unique opportunity to uncover common signaling mechanisms that may be important for regeneration of respiratory organs in all vertebrates. This may lead to new advances in tissue repair following lung disease.

scholarly journals FLOWERING LOCUS T genes control onion bulb formation and flowering

2013 ◽  
Vol 4 (1) ◽  
Author(s):  
Robyn Lee ◽  
Samantha Baldwin ◽  
Fernand Kenel ◽  
John McCallum ◽  
Richard Macknight
Keyword(s):  
Onion Bulb ◽  
Flowering Locus T ◽  
Bulb Formation ◽  
Onion Bulb Formation ◽  
Flowering Locus

scholarly journals Dynamic Crosstalk between Vascular Smooth Muscle Cells and the Aged Extracellular Matrix

2021 ◽  
Vol 22 (18) ◽  
pp. 10175
Author(s):  
Joao Carlos Ribeiro-Silva ◽  
Patricia Nolasco ◽  
Jose Eduardo Krieger ◽  
Ayumi Aurea Miyakawa
Keyword(s):  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Elastic Fibers ◽  
Signaling Mechanisms ◽  
Arterial Aging ◽  
Underlying Mechanisms ◽  
Cell Phenotypes

Vascular aging is accompanied by the fragmentation of elastic fibers and collagen deposition, leading to reduced distensibility and increased vascular stiffness. A rigid artery facilitates elastin to degradation by MMPs, exposing vascular cells to greater mechanical stress and triggering signaling mechanisms that only exacerbate aging, creating a self-sustaining inflammatory environment that also promotes vascular calcification. In this review, we highlight the role of crosstalk between smooth muscle cells and the vascular extracellular matrix (ECM) and how aging promotes smooth muscle cell phenotypes that ultimately lead to mechanical impairment of aging arteries. Understanding the underlying mechanisms and the role of associated changes in ECM during aging may contribute to new approaches to prevent or delay arterial aging and the onset of cardiovascular diseases.

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