scholarly journals STEM-10. MOLECULAR MECHANISMS UNDERLYING PHENOTYPIC PLASTICITY IN MALIGNANT GLIOMA

2018 ◽  
Vol 20 (suppl_6) ◽  
pp. vi245-vi246
Author(s):  
Costanza LoCascio ◽  
Ernesto Luna-Melendez ◽  
Shwetal Mehta
Keyword(s):  
Phenotypic Plasticity ◽  
Malignant Glioma ◽  
Molecular Mechanisms

Molecular mechanisms of phenotypic plasticity in social insects

2016 ◽  
Vol 13 ◽  
pp. 55-60 ◽  
Author(s):  
Miguel Corona ◽  
Romain Libbrecht ◽  
Diana E Wheeler
Keyword(s):  
Phenotypic Plasticity ◽  
Social Insects ◽  
Molecular Mechanisms

scholarly journals Ecdysone signaling underlies the pea aphid transgenerational wing polyphenism

2017 ◽  
Vol 114 (6) ◽  
pp. 1419-1423 ◽  
Author(s):  
Neetha Nanoth Vellichirammal ◽  
Purba Gupta ◽  
Tannice A. Hall ◽  
Jennifer A. Brisson
Keyword(s):  
Phenotypic Plasticity ◽  
Molecular Mechanisms ◽  
Receptor Gene ◽  
Expression Patterns ◽  
Pea Aphid ◽  
Laboratory Model ◽  
Causative Role ◽  
Ecdysone Receptor ◽  
Aphid Density ◽  
Ecdysone Signaling

The wing polyphenism of pea aphids is a compelling laboratory model with which to study the molecular mechanisms underlying phenotypic plasticity. In this polyphenism, environmental stressors such as high aphid density cause asexual, viviparous adult female aphids to alter the developmental fate of their embryos from wingless to winged morphs. This polyphenism is transgenerational, in that the pea aphid mother experiences the environmental signals, but it is her offspring that are affected. Previous research suggested that the steroid hormone ecdysone may play a role in this polyphenism. Here, we analyzed ecdysone-related gene expression patterns and found that they were consistent with a down-regulation of the ecdysone pathway being involved in the production of winged offspring. We therefore predicted that reduced ecdysone signaling would result in more winged offspring. Experimental injections of ecdysone or its analog resulted in a decreased production of winged offspring. Conversely, interfering with ecdysone signaling using an ecdysone receptor antagonist or knocking down the ecdysone receptor gene with RNAi resulted in an increased production of winged offspring. Our results are therefore consistent with the idea that ecdysone plays a causative role in the regulation of the proportion of winged offspring produced in response to crowding in this polyphenism. Our results also show that an environmentally regulated maternal hormone can mediate phenotype production in the next generation, as well as provide significant insight into the molecular mechanisms underlying the functioning of transgenerational phenotypic plasticity.

scholarly journals Epithelial-mesenchymal plasticity: How have quantitative mathematical models helped improve our understanding?

2017 ◽  
Author(s):  
Mohit Kumar Jolly ◽  
Satyendra C Tripathi ◽  
Jason A Somarelli ◽  
Samir M Hanash ◽  
Herbert Levine
Keyword(s):  
Phenotypic Plasticity ◽  
Mathematical Models ◽  
Tumor Progression ◽  
Immune Evasion ◽  
Molecular Mechanisms ◽  
Invasion And Metastasis ◽  
Hallmarks Of Cancer ◽  
Mesenchymal Phenotype ◽  
Extracellular Signals ◽  
Clinical Challenge

AbstractPhenotypic plasticity, the ability of cells to reversibly alter their phenotypes in response to signals, presents a significant clinical challenge to treating solid tumors. Tumor cells utilize phenotypic plasticity to evade therapies, metastasize, and colonize distant organs. As a result, phenotypic plasticity can accelerate tumor progression. A well-studied example of phenotypic plasticity is the bidirectional conversions among epithelial, mesenchymal, and hybrid epithelial/mesenchymal phenotype(s). These conversions can alter a repertoire of cellular traits associated with multiple hallmarks of cancer, such as metabolism, immune-evasion, and invasion and metastasis. To tackle the complexity and heterogeneity of these transitions, mathematical models have been developed that seek to capture the experimentally-verified molecular mechanisms and act as ‘ hypothesis-generating machines’. Here, we discuss how these quantitative mathematical models have helped us explain existing experimental data, guided further experiments, and provided an improved conceptual framework for understanding how multiple intracellular and extracellular signals can drive epithelial-mesenchymal plasticity at both the single-cell and population levels. We also discuss the implications of this plasticity in driving multiple aggressive facets of tumor progression.

scholarly journals Epigenetic Influences on Plant Responses to the Environment [University of Wisconsin - Oshkosh]

2019 ◽  
Author(s):  
Angela L Vickman ◽  
Travis Smith ◽  
Hayley Vandenboom ◽  
Lisa A. Dorn
Keyword(s):  
Gene Expression ◽  
Phenotypic Plasticity ◽  
Molecular Mechanisms ◽  
Molecular Level ◽  
Physical Structure ◽  
Plant Responses ◽  
Appropriate Behavior ◽  
Stressful Environment ◽  
University Of Wisconsin

Plants and animals may respond to changes in the environment at the molecular level by changing the amount of a gene product (a protein) to generate the appropriate behavior or physical structure (a phenotype) for that environment. For example, an extremely stressful environment can cause plants to reproduce immediately rather than waiting for conditions to improve. The molecular mechanisms for changing phenotype with environment (phenotypic plasticity) are not clear, however previous studies have shown plasticity may be the result of failing to change expression to maintain a phenotype or a deliberate change in expression altering the phenotype. To explore the molecular mechanisms underlying phenotypic plasticity, I am using a minION sequencing apparatus to re-sequence three inbred lines of Arabidopsis thaliana with extreme phenotypic plasticity differences and gene expression differences with the environment. I will specifically explore the role of methylated cytosines and adenines in gene expression.

scholarly journals Histone acetylation regulates the expression of genes involved in worker reproduction in the ant Temnothorax rugatulus

BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Marina Choppin ◽  
Barbara Feldmeyer ◽  
Susanne Foitzik
Keyword(s):  
Phenotypic Plasticity ◽  
Histone Acetylation ◽  
Social Insects ◽  
Molecular Mechanisms ◽  
Fat Body ◽  
Antioxidant Properties ◽  
Worker Reproduction ◽  
Ovary Development ◽  
Chemical Inhibitors

Abstract Background In insect societies, queens monopolize reproduction while workers perform tasks such as brood care or foraging. Queen loss leads to ovary development and lifespan extension in workers of many ant species. However, the underlying molecular mechanisms of this phenotypic plasticity remain unclear. Recent studies highlight the importance of epigenetics in regulating plastic traits in social insects. Thus, we investigated the role of histone acetylation in regulating worker reproduction in the ant Temnothorax rugatulus. We removed queens from their colonies to induce worker fecundity, and either fed workers with chemical inhibitors of histone acetylation (C646), deacetylation (TSA), or the solvent (DMSO) as control. We monitored worker number for six weeks after which we assessed ovary development and sequenced fat body mRNA. Results Workers survived better in queenless colonies. They also developed their ovaries after queen removal in control colonies as expected, but not in colonies treated with the chemical inhibitors. Both inhibitors affected gene expression, although the inhibition of histone acetylation using C646 altered the expression of more genes with immunity, fecundity, and longevity functionalities. Interestingly, these C646-treated workers shared many upregulated genes with infertile workers from queenright colonies. We also identified one gene with antioxidant properties commonly downregulated in infertile workers from queenright colonies and both C646 and TSA-treated workers from queenless colonies. Conclusion Our results suggest that histone acetylation is involved in the molecular regulation of worker reproduction, and thus point to an important role of histone modifications in modulating phenotypic plasticity of life history traits in social insects.

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