Do the microRNAs we eat affect gene expression?

Nature ◽  
2020 ◽  
Vol 582 (7812) ◽  
pp. S10-S11 ◽  
Author(s):  
Kristina Campbell
Keyword(s):  
Gene Expression ◽  
Affect Gene Expression

Phenotypic plasticity

2018 ◽  
Author(s):  
Karen D. Williams ◽  
Marla B. Sokolowski
Keyword(s):  
Gene Expression ◽  
Phenotypic Plasticity ◽  
Environmental Change ◽  
Behavioral Plasticity ◽  
Behavioral Flexibility ◽  
Insect Behavior ◽  
Behavioral Variability ◽  
Gene By Environment Interactions ◽  
Affect Gene Expression

Why is there so much variation in insect behavior? This chapter will address the sources of behavioral variability, with a particular focus on phenotypic plasticity. Variation in social, nutritional, and seasonal environmental contexts during development and adulthood can give rise to phenotypic plasticity. To delve into mechanism underlying behavioral flexibility in insects, examples of polyphenisms, a type of phenotypic plasticity, will be discussed. Selected examples reveal that environmental change can affect gene expression, which in turn can affect behavioral plasticity. These changes in gene expression together with gene-by-environment interactions are discussed to illuminate our understanding of insect behavioral plasticity.

scholarly journals Concerted genomic and epigenomic changes accompany stabilization of Arabidopsis allopolyploids

2021 ◽  
Vol 5 (10) ◽  
pp. 1382-1393
Author(s):  
Xinyu Jiang ◽  
Qingxin Song ◽  
Wenxue Ye ◽  
Z. Jeffrey Chen
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Small Rnas ◽  
Structural Variation ◽  
Self Incompatibility ◽  
Polyploid Evolution ◽  
Genomic Variations ◽  
Conserved Gene ◽  
Arabidopsis Suecica ◽  
Affect Gene Expression

AbstractDuring evolution successful allopolyploids must overcome ‘genome shock’ between hybridizing species but the underlying process remains elusive. Here, we report concerted genomic and epigenomic changes in resynthesized and natural Arabidopsis suecica (TTAA) allotetraploids derived from Arabidopsisthaliana (TT) and Arabidopsisarenosa (AA). A. suecica shows conserved gene synteny and content with more gene family gain and loss in the A and T subgenomes than respective progenitors, although A. arenosa-derived subgenome has more structural variation and transposon distributions than A. thaliana-derived subgenome. These balanced genomic variations are accompanied by pervasive convergent and concerted changes in DNA methylation and gene expression among allotetraploids. The A subgenome is hypomethylated rapidly from F1 to resynthesized allotetraploids and convergently to the T-subgenome level in natural A. suecica, despite many other methylated loci being inherited from F1 to all allotetraploids. These changes in DNA methylation, including small RNAs, in allotetraploids may affect gene expression and phenotypic variation, including flowering, silencing of self-incompatibility and upregulation of meiosis- and mitosis-related genes. In conclusion, concerted genomic and epigenomic changes may improve stability and adaptation during polyploid evolution.

scholarly journals Mammalian linker-histone subtypes differentially affect gene expression in vivo

2003 ◽  
Vol 100 (10) ◽  
pp. 5920-5925 ◽  
Author(s):  
R. Alami ◽  
Y. Fan ◽  
S. Pack ◽  
T. M. Sonbuchner ◽  
A. Besse ◽  
...  
Keyword(s):  
Gene Expression ◽  
Linker Histone ◽  
Affect Gene Expression

scholarly journals Pathogenic copy number variants that affect gene expression contribute to genomic burden in cerebral palsy

2018 ◽  
Vol 3 (1) ◽  
Author(s):  
Mark A. Corbett ◽  
Clare L. van Eyk ◽  
Dani L. Webber ◽  
Stephen J. Bent ◽  
Morgan Newman ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cerebral Palsy ◽  
Copy Number ◽  
Copy Number Variants ◽  
Affect Gene Expression

scholarly journals Enhancer variants associated with Alzheimer’s disease affect gene expression via chromatin looping

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Masataka Kikuchi ◽  
Norikazu Hara ◽  
Mai Hasegawa ◽  
Akinori Miyashita ◽  
Ryozo Kuwano ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Regulatory Elements ◽  
Genome Wide Association Studies ◽  
Expression Levels ◽  
Chromatin Loops ◽  
Coding Regions ◽  
Affect Gene Expression ◽  
Gene Expression Levels

Abstract Background Genome-wide association studies (GWASs) have identified single-nucleotide polymorphisms (SNPs) that may be genetic factors underlying Alzheimer’s disease (AD). However, how these AD-associated SNPs (AD SNPs) contribute to the pathogenesis of this disease is poorly understood because most of them are located in non-coding regions, such as introns and intergenic regions. Previous studies reported that some disease-associated SNPs affect regulatory elements including enhancers. We hypothesized that non-coding AD SNPs are located in enhancers and affect gene expression levels via chromatin loops. Methods To characterize AD SNPs within non-coding regions, we extracted 406 AD SNPs with GWAS p-values of less than 1.00 × 10− 6 from the GWAS catalog database. Of these, we selected 392 SNPs within non-coding regions. Next, we checked whether those non-coding AD SNPs were located in enhancers that typically regulate gene expression levels using publicly available data for enhancers that were predicted in 127 human tissues or cell types. We sought expression quantitative trait locus (eQTL) genes affected by non-coding AD SNPs within enhancers because enhancers are regulatory elements that influence the gene expression levels. To elucidate how the non-coding AD SNPs within enhancers affect the gene expression levels, we identified chromatin-chromatin interactions by Hi-C experiments. Results We report the following findings: (1) nearly 30% of non-coding AD SNPs are located in enhancers; (2) eQTL genes affected by non-coding AD SNPs within enhancers are associated with amyloid beta clearance, synaptic transmission, and immune responses; (3) 95% of the AD SNPs located in enhancers co-localize with their eQTL genes in topologically associating domains suggesting that regulation may occur through chromatin higher-order structures; (4) rs1476679 spatially contacts the promoters of eQTL genes via CTCF-CTCF interactions; (5) the effect of other AD SNPs such as rs7364180 is likely to be, at least in part, indirect through regulation of transcription factors that in turn regulate AD associated genes. Conclusion Our results suggest that non-coding AD SNPs may affect the function of enhancers thereby influencing the expression levels of surrounding or distant genes via chromatin loops. This result may explain how some non-coding AD SNPs contribute to AD pathogenesis.

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