During growth and development, plants undergo a series of phase transitions from the juvenile-to-adult vegetative phase to the reproductive phase. In Arabidopsis, vegetative phase transitions and flowering are regulated by SQUAMOSA PROMOTER BINDING PROTEIN-LIKE (SPL) factors. SPL mRNAs are post-transcriptionally regulated by miR156 in an age-dependent manner; however, the role of other mechanisms in this process is not known. In this study, we demonstrate that the HAG1/GCN5- and PRZ1/ADA2b-containing SAGA-like histone acetyltransferase (HAT) complex directly controls the transcription of SPLs and determines the time for juvenile-to-adult phase transition. Thus, epigenetic control by the SAGA-like HAT complex determines the transcriptional output of SPLs, which might be a prerequisite for the subsequent post-transcriptional regulation by miR156. Importantly, this epigenetic control mechanism is also crucial for miR156-independent induction of SPLs and acceleration of phase transition by light and photoperiod or during post-embryonic growth.
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http://dx.doi.org/10.1111/tpj.12908 | DOI Listing |
INhibitor of Growth (ING1-5) proteins are epigenetic readers that target histone acetyltransferase (HAT) or histone deacetylase (HDAC) complexes to the H3K4Me3 mark of active transcription. ING5 targets Moz/Morf and HBO1 HAT complexes that alter acetylation of H3 and H4 core histones, affecting gene expression. Previous experiments in vitro indicated that ING5 functions to maintain stem cell character in normal and in cancer stem cells.
View Article and Find Full Text PDFEur J Epidemiol
January 2025
Department of Psychiatry, Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, 800 E. Leigh St., Suite 100, Richmond, VA, 23298, USA.
Cigarette smoking is associated with numerous differentially-methylated genomic loci in multiple human tissues. These associations are often assumed to reflect the causal effects of smoking on DNA methylation (DNAm), which may underpin some of the adverse health sequelae of smoking. However, prior causal analyses with Mendelian Randomisation (MR) have found limited support for such effects.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Background: Despite age being the primary risk factor for Alzheimer's disease (AD), there remains a necessity for a thorough understanding of the distinct biological pathways affected in the course of healthy aging as opposed to the pathological aging that leads to neurodegeneration. As the genome remains constant throughout one's lifespan, it becomes crucial to unravel the impact of aging on the proteome. Proteins, being key players in various cellular functions, mediate the effects of environmental stimuli and epigenetic alterations.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
John P. Hussman Institute for Human Genomics, University of Miami Miller School of Medicine, Miami, FL, USA.
Background: Sex is an important factor that contributes to both clinical and biological heterogeneity in Alzheimer's disease (AD), but the regulatory mechanisms underlying sex differences in AD are still not well understood. DNA methylation (DNAm) is an epigenetic modification that regulates gene transcription and is known to be involved in AD. However, due to analytical and biological complexity, few previous DNAm studies analyzed the X chromosome, where many genes influencing cognitive abilities and immune functions are located.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Edith Cowan University, Joondalup, Australia; Australian E-Health Research Centre, CSIRO, Perth, Western Australia, Australia.
Background: A growing body of research has confirmed the presence of epigenetic alterations in Alzheimer's disease (AD). While the causal relationship between these changes and AD remains uncertain, they offer a novel avenue to explore potential treatments. In this study, we aimed at characterising the methylation signatures of amyloid beta (Aβ) deposition, one of the main hallmarks of AD.
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