scholarly journals Mechanisms driving endosperm-based hybrid incompatibilities: insights from hybrid monkeyflowers

2018 ◽  
Author(s):  
Taliesin J. Kinser ◽  
Ronald D. Smith ◽  
Amelia H. Lawrence ◽  
Arielle M. Cooley ◽  
Mario Vallejo-Marin ◽  
...  

ABSTRACTAngiosperm endosperm requires genomic and epigenomic interactions between maternal and paternal genomes for proper seed development. Genomic imprinting, an epigenetic phenomenon where the expression of certain genes is predominantly contributed by one parent, is an essential part of this process and unique to endosperm. Perturbation of imprinting can be fatal to developing seeds, and can be caused by interspecific or interploidy hybridization. However, underlying mechanisms driving these endosperm-based hybridization barriers are not well understood or described. Here we investigate the consequences of genomic imprinting in a naturally occurring interploidy and interspecies hybrid between the diploid, Mimulus guttatus, and the allotetraploid (with two subgenomes), M. luteus (Phrymaceae). We find that the two parental species differ in patterns of DNA methylation, gene expression, and imprinting. Hybrid crosses in both directions, which suffer from endosperm abnormalities and decreased germination rates, display altered methylation patterns compared to parent endosperm. Furthermore, imprinting and expression patterns appear perturbed in hybrid endosperm, where we observe global expression dominance of each of the two M. luteus subgenomes, which share similar expression patterns, over the M. guttatus genome, regardless of crossing direction. We suggest that epigenetic repatterning within the hybrid may drive global shifts in expression patterns and be the result of diverged epigenetic/regulatory landscapes between parental genomes. This may either establish or exacerbate dosage-based epistatic incompatibilities between the specific imprinting patterns that have diverged between parental species, thus driving potentially rapid endosperm-based hybridization barriers.

Author(s):  
Dragan Stajic ◽  
Lars E. T. Jansen

The cellular machinery that regulates gene expression can be self-propagated across cell division cycles and even generations. This renders gene expression states and their associated phenotypes heritable, independently of genetic changes. These phenotypic states, in turn, can be subject to selection and may influence evolutionary adaptation. In this review, we will discuss the molecular basis of epigenetic inheritance, the extent of its transmission and mechanisms of evolutionary adaptation. The current work shows that heritable gene expression can facilitate the process of adaptation through the increase of survival in a novel environment and by enlarging the size of beneficial mutational targets. Moreover, epigenetic control of gene expression enables stochastic switching between different phenotypes in populations that can potentially facilitate adaptation in rapidly fluctuating environments. Ecological studies of the variation of epigenetic markers (e.g. DNA methylation patterns) in wild populations show a potential contribution of this mode of inheritance to local adaptation in nature. However, the extent of the adaptive contribution of the naturally occurring variation in epi-alleles compared to genetic variation remains unclear.This article is part of the theme issue ‘How does epigenetics influence the course of evolution?’


2019 ◽  
Author(s):  
Yuancheng Lu ◽  
Anitha Krishnan ◽  
Benedikt Brommer ◽  
Xiao Tian ◽  
Margarita Meer ◽  
...  

Ageing is a degenerative process leading to tissue dysfunction and death. A proposed cause of ageing is the accumulation of epigenetic noise, which disrupts youthful gene expression patterns that are required for cells to function optimally and recover from damage1–3. Changes to DNA methylation patterns over time form the basis of an ‘ageing clock’4, 5, but whether old individuals retain information to reset the clock and, if so, whether this would improve tissue function is not known. Of all the tissues in the body, the central nervous system (CNS) is one of the first to lose regenerative capacity6, 7. Using the eye as a model tissue, we show that expression of Oct4, Sox2, and Klf4 genes (OSK) in mice resets youthful gene expression patterns and the DNA methylation age of retinal ganglion cells, promotes axon regeneration after optic nerve crush injury, and restores vision in a mouse model of glaucoma and in normal old mice. This process, which we call recovery of information via epigenetic reprogramming or REVIVER, requires the DNA demethylases Tet1 and Tet2, indicating that DNA methylation patterns don’t just indicate age, they participate in ageing. Thus, old tissues retain a faithful record of youthful epigenetic information that can be accessed for functional age reversal.


Agronomy ◽  
2020 ◽  
Vol 10 (10) ◽  
pp. 1484
Author(s):  
Clémentine Mercé ◽  
Philipp E. Bayer ◽  
Cassandria Tay Fernandez ◽  
Jacqueline Batley ◽  
David Edwards

The methylation of gene promoters is an epigenetic process that can have a major impact on plant phenotypes through its control of gene expression. This phenomenon can be observed as a response to stress, such as drought, cold/heat stress or pathogen infection. The transgenerational heritability of DNA methylation marks could enable breeders to fix beneficial methylation patterns in crops over successive generations. These properties of DNA methylation, its impact on the phenotype and its heritability, could be used to support the accelerated breeding of improved crop varieties. Induced DNA methylation has the potential to complement the existing plant breeding process, supporting the introduction of desirable characteristics in crops within a single generation that persist in its progeny. Therefore, it is important to understand the underlying mechanisms involved in the regulation of gene expression through DNA methylation and to develop methods for precisely modulating methylation patterns for crop improvement. Here we describe the currently available epigenetic editing tools and their advantages and limitations in the domain of crop breeding. Finally, we discuss the biological and legislative limitations currently restricting the development of epigenetic modification as a crop improvement tool.


2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Dengwei Zhang ◽  
Si Zhou ◽  
Ziheng Zhou ◽  
Xiaosen Jiang ◽  
Dongsheng Chen ◽  
...  

Abstract Background Birth defects pose a major challenge to infant health. Thus far, however, the causes of most birth defects remain cryptic. Over the past few decades, considerable effort has been expended on disclosing the underlying mechanisms related to birth defects, yielding myriad treatises and data. To meet the increasing requirements for data resources, we developed a freely accessible birth defect multi-omics database (BDdb, http://t21omics.cngb.org) consisting of multi-omics data and potential disease biomarkers. Results In total, omics datasets from 136 Gene Expression Omnibus (GEO) Series records, including 5245 samples, as well as 869 biomarkers of 22 birth defects in six different species, were integrated into the BDdb. The database provides a user-friendly interface for searching, browsing, and downloading data of interest. The BDdb also enables users to explore the correlations among different sequencing methods, such as chromatin immunoprecipitation sequencing (ChIP-Seq) and RNA sequencing (RNA-Seq) from different studies, to obtain the information on gene expression patterns from diverse aspects. Conclusion To the best of our knowledge, the BDdb is the first comprehensive database associated with birth defects, which should benefit the diagnosis and prevention of birth defects.


2017 ◽  
Author(s):  
Jeremy Pasquier ◽  
Ingo Braasch ◽  
Peter Batzel ◽  
Cedric Cabau ◽  
Jérome Montfort ◽  
...  

AbstractWhole genome duplications (WGD) are important evolutionary events. Our understanding of underlying mechanisms, including the evolution of duplicated genes after WGD, however remains incomplete. Teleost fish experienced a common WGD (teleost-specific genome duplication, or TGD) followed by a dramatic adaptive radiation leading to more than half of all vertebrate species. The analysis of gene expression patterns following TGD at the genome level has been limited by the lack of suitable genomic resources. The recent concomitant release of the genome sequence of spotted gar (a representative of holosteans, the closest lineage of teleosts that lacks the TGD) and the tissue-specific gene expression repertoires of over 20 holostean and teleostean fish species, including spotted gar, zebrafish and medaka (the PhyloFish project), offered a unique opportunity to study the evolution of gene expression following TGD in teleosts. We show that most TGD duplicates gained their current status (loss of one duplicate gene or retention of both duplicates) relatively rapidly after TGD (i.e. prior to the divergence of medaka and zebrafish lineages). The loss of one duplicate is the most common fate after TGD with a probability of approximately 80%. In addition, the fate of duplicate genes after TGD, including subfunctionalization, neofunctionalization, or retention of two ‘similar’ copies occurred not only before, but also after the radiation of species tested, in consistency with a role of the TGD in speciation and/or evolution of gene function. Finally, we report novel cases of TGD ohnolog subfunctionalization and neofunctionalization that further illustrate the importance of these processes.


2021 ◽  
Vol 12 ◽  
Author(s):  
Nazia Parveen ◽  
Sangeeta Dhawan

Pancreatic beta cells play a central role in regulating glucose homeostasis by secreting the hormone insulin. Failure of beta cells due to reduced function and mass and the resulting insulin insufficiency can drive the dysregulation of glycemic control, causing diabetes. Epigenetic regulation by DNA methylation is central to shaping the gene expression patterns that define the fully functional beta cell phenotype and regulate beta cell growth. Establishment of stage-specific DNA methylation guides beta cell differentiation during fetal development, while faithful restoration of these signatures during DNA replication ensures the maintenance of beta cell identity and function in postnatal life. Lineage-specific transcription factor networks interact with methylated DNA at specific genomic regions to enhance the regulatory specificity and ensure the stability of gene expression patterns. Recent genome-wide DNA methylation profiling studies comparing islets from diabetic and non-diabetic human subjects demonstrate the perturbation of beta cell DNA methylation patterns, corresponding to the dysregulation of gene expression associated with mature beta cell state in diabetes. This article will discuss the molecular underpinnings of shaping the islet DNA methylation landscape, its mechanistic role in the specification and maintenance of the functional beta cell phenotype, and its dysregulation in diabetes. We will also review recent advances in utilizing beta cell specific DNA methylation patterns for the development of biomarkers for diabetes, and targeting DNA methylation to develop translational approaches for supplementing the functional beta cell mass deficit in diabetes.


2021 ◽  
Vol 12 ◽  
Author(s):  
Umair Ali Khan Saddozai ◽  
Fengling Wang ◽  
Muhammad Usman Akbar ◽  
Lu Zhang ◽  
Yang An ◽  
...  

Pheochromocytoma (PCC) is a rare neuroendocrine tumor of the adrenal gland with a high rate of mortality if diagnosed at a late stage. Common symptoms of pheochromocytoma include headache, anxiety, palpitation, and diaphoresis. Different treatments are under observation for PCC but there is still no effective treatment option. Recently, the gene expression profiling of various tumors has provided new subtype-specific options for targeted therapies. In this study, using data sets from TCGA and the GSE19422 cohorts, we identified two distinct PCC subtypes with distinct gene expression patterns. Genes enriched in Subtype I PCCs were involved in the dopaminergic synapse, nicotine addiction, and long-term depression pathways, while genes enriched in subtype II PCCs were involved in protein digestion and absorption, vascular smooth muscle contraction, and ECM receptor interaction pathways. We further identified subtype specific genes such as ALK, IGF1R, RET, and RSPO2 for subtype I and EGFR, ESR1, and SMO for subtype II, the overexpression of which led to cell invasion and tumorigenesis. These genes identified in the present research may serve as potential subtype-specific therapeutic targets to understand the underlying mechanisms of tumorigenesis. Our findings may further guide towards the development of targeted therapies and potential molecular biomarkers against PCC.


Genes ◽  
2021 ◽  
Vol 12 (8) ◽  
pp. 1153
Author(s):  
Nicole Robles-Matos ◽  
Tre Artis ◽  
Rebecca A. Simmons ◽  
Marisa S. Bartolomei

Genomic imprinting is an epigenetic mechanism that results in monoallelic, parent-of-origin-specific expression of a small number of genes. Imprinted genes play a crucial role in mammalian development as their dysregulation result in an increased risk of human diseases. DNA methylation, which undergoes dynamic changes early in development, is one of the epigenetic marks regulating imprinted gene expression patterns during early development. Thus, environmental insults, including endocrine disrupting chemicals during critical periods of fetal development, can alter DNA methylation patterns, leading to inappropriate developmental gene expression and disease risk. Here, we summarize the current literature on the impacts of in utero exposure to endocrine disrupting chemicals on genomic imprinting and metabolism in humans and rodents. We evaluate how early-life environmental exposures are a potential risk factor for adult metabolic diseases. We also introduce our mouse model of phthalate exposure. Finally, we describe the potential of genomic imprinting to serve as an environmental sensor during early development and as a novel biomarker for postnatal health outcomes.


2013 ◽  
Vol 33 (6) ◽  
pp. 629-637 ◽  
Author(s):  
K-H Liu ◽  
C-P Wang ◽  
M-F Chang ◽  
Y-W Chung ◽  
P-J Lou ◽  
...  

Photodynamic therapy (PDT) is a novel cancer treatment based on the tumor-specific accumulation of a photosensitizer followed by irradiation with visible light, which induces selective tumor cell death via production of reactive oxygen species. To elucidate the underlying mechanisms, microarray analysis was used to analyze the changes in gene expression patterns during PDT induced by various photosensitizers. Cancer cells were subjected to four different photosensitizer-mediated PDT and the resulting gene expression profiles were compared. We identified many differentially expressed genes reported previously as well as new genes for which the functionfunctions in PDT are still unclear. Our current results not only advance the general understanding of PDT but also suggest that distinct molecular mechanisms are involved in different photosensitizer-mediated PDT. Elucidating the signaling mechanisms in PDT will provide information to modulate the antitumor effectiveness of PDT using various photosensitizers.


2012 ◽  
Vol 24 (1) ◽  
pp. 45 ◽  
Author(s):  
Cheryl S. Rosenfeld

Maternal diet and secondary factors can strikingly influence fetal outcomes, including biasing offspring sex ratio and altering the molecular biological responses of the conceptus, namely within the placenta. Alterations in the in utero environment might also lead to profound developmental origin of health and disease (DOHaD) outcomes into adulthood, including increased risk for cardiovascular disease, obesity and cancer, with males in general being at greater risk for these diseases. Female mice maintained on a very high fat (VHF) diet birth more sons than those on a chow-based and low fat (LF), high carbohydrate diet, with the latter group producing more daughters. However, neither the underlying mechanisms that contribute to this shift in offspring sex ratio nor when they occur during pregnancy have been resolved. In this review, we consider the evidence that maternal diet and other factors influence secondary sex ratio in a variety of species, including humans, and discuss when this skewing might occur. Additionally, we examine how fetal sex and maternal diet influences gene expression patterns in the mouse placenta, which serves as the primary nutrient acquisition and communication organ between the mother and her developing pups. These adaptations to diet observed as changes in gene expression are likely to provide insight into how the placenta buffers the fetus proper from environmental shifts in nutrient availability during pregnancy and whether male and female conceptuses respond differently to such challenges.


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