scholarly journals X chromosome-dependent disruption of placental regulatory networks in hybrid dwarf hamsters

Genetics ◽  
2021 ◽  
Author(s):  
Thomas D Brekke ◽  
Emily C Moore ◽  
Shane C Campbell-Staton ◽  
Colin M Callahan ◽  
Zachary A Cheviron ◽  
...  
Keyword(s):  
Gene Expression ◽  
X Chromosome ◽  
Regulatory Networks ◽  
Mammalian Species ◽  
Strongly Correlated ◽  
Placental Development ◽  
Substitution Lines ◽  
Genome Wide ◽  
Highly Sensitive ◽  
First And Second Generation

AbstractEmbryonic development in mammals is highly sensitive to changes in gene expression within the placenta. The placenta is also highly enriched for genes showing parent-of-origin or imprinted expression, which is predicted to evolve rapidly in response to parental conflict. However, little is known about the evolution of placental gene expression, or if divergence of placental gene expression plays an important role in mammalian speciation. We used crosses between two species of dwarf hamsters (Phodopus sungorus and Phodopus campbelli) to examine the genetic and regulatory underpinnings of severe placental overgrowth in their hybrids. Using quantitative genetic mapping and mitochondrial substitution lines, we show that overgrowth of hybrid placentas was primarily caused by genetic differences on the maternally inherited P. sungorus X chromosome. Mitochondrial interactions did not contribute to abnormal hybrid placental development, and there was only weak correspondence between placental disruption and embryonic growth. Genome-wide analyses of placental transcriptomes from the parental species and first- and second-generation hybrids revealed a central group of co-expressed X-linked and autosomal genes that were highly enriched for maternally biased expression. Expression of this gene network was strongly correlated with placental size and showed widespread misexpression dependent on epistatic interactions with X-linked hybrid incompatibilities. Collectively, our results indicate that the X chromosome is likely to play a prominent role in the evolution of placental gene expression and the accumulation of hybrid developmental barriers between mammalian species.

scholarly journals X chromosome-dependent disruption of placental regulatory networks in hybrid dwarf hamsters

2020 ◽  
Author(s):  
Thomas D. Brekke ◽  
Emily C. Moore ◽  
Shane C. Campbell-Staton ◽  
Colin M. Callahan ◽  
Zachary A. Cheviron ◽  
...  
Keyword(s):  
Gene Expression ◽  
X Chromosome ◽  
Regulatory Networks ◽  
Mammalian Species ◽  
Strongly Correlated ◽  
Placental Development ◽  
Substitution Lines ◽  
Genome Wide ◽  
Highly Sensitive ◽  
First And Second Generation

Embryonic development in mammals is highly sensitive to changes in gene expression within the placenta. The placenta is also highly enriched for genes showing parent-of-origin or imprinted expression, which is predicted to evolve rapidly in response to parental conflict. However, little is known about the evolution of placental gene expression, or if divergence of placental gene expression plays an important role in mammalian speciation. We used crosses between two species of dwarf hamsters (Phodopus sungorus and P. campbelli) to examine the genetic and regulatory underpinnings of severe placental overgrowth. Using quantitative genetic mapping and mitochondrial substitution lines, we show that overgrowth of hybrid placenta was primarily caused by genetic differences on the maternally inherited P. sungorus X chromosome. Mitochondrial interactions did not contribute to abnormal hybrid placental development, and there was only weak correspondence between placental disruption and embryonic growth. Genome-wide analyses of placental transcriptomes from the parental species and first and second-generation hybrids revealed a central group of co-expressed X-linked and autosomal genes that were highly enriched for maternally-biased expression. Expression of this gene network was strongly correlated with placental size and showed widespread misexpression dependent on epistatic interactions with X-linked hybrid incompatibilities. Collectively, our results indicate that the X chromosome plays a prominent role in the evolution of placental gene expression and the rapid accumulation of hybrid developmental barriers between mammalian species.

scholarly journals Diverse developmental strategies of X chromosome dosage compensation in eutherian mammals

2019 ◽  
Vol 63 (3-4-5) ◽  
pp. 223-233 ◽  
Author(s):  
Alexander I. Shevchenko ◽  
Elena V. Dementyeva ◽  
Irina S. Zakharova ◽  
Suren M. Zakian
Keyword(s):  
Gene Expression ◽  
X Chromosome ◽  
Dosage Compensation ◽  
Mammalian Species ◽  
X Chromosome Inactivation ◽  
Chromosome Inactivation ◽  
Autosomal Gene ◽  
Mammalian Development ◽  
Compensation Mechanisms ◽  
Early Mammalian Development

In eutherian mammals, dosage compensation arose to balance X-linked gene expression between sexes and relatively to autosomal gene expression in the evolution of sex chromosomes. Dosage compensation occurs in early mammalian development and comprises X chromosome upregulation and inactivation that are tightly coordinated epigenetic processes. Despite a uniform principle of dosage compensation, mechanisms of X chromosome inactivation and upregulation demonstrate a significant variability depending on sex, developmental stage, cell type, individual, and mammalian species. The review focuses on relationships between X chromosome inactivation and upregulation in mammalian early development.

Identification of early gene expression changes during human Th17 cell differentiation

Blood ◽  
2012 ◽  
Vol 119 (23) ◽  
pp. e151-e160 ◽  
Author(s):  
Soile Tuomela ◽  
Verna Salo ◽  
Subhash K. Tripathi ◽  
Zhi Chen ◽  
Kirsti Laurila ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Differentiation ◽  
Th17 Cell ◽  
Regulatory Networks ◽  
Molecular Mechanisms ◽  
Early Gene ◽  
Th17 Cell Differentiation ◽  
Genome Wide ◽  
Starting Point ◽  
Th17 Differentiation

Abstract Th17 cells play an essential role in the pathogenesis of autoimmune and inflammatory diseases. Most of our current understanding on Th17 cell differentiation relies on studies carried out in mice, whereas the molecular mechanisms controlling human Th17 cell differentiation are less well defined. In this study, we identified gene expression changes characterizing early stages of human Th17 cell differentiation through genome-wide gene expression profiling. CD4+ cells isolated from umbilical cord blood were used to determine detailed kinetics of gene expression after initiation of Th17 differentiation with IL1β, IL6, and TGFβ. The differential expression of selected candidate genes was further validated at protein level and analyzed for specificity in initiation of Th17 compared with initiation of other Th subsets, namely Th1, Th2, and iTreg. This first genome-wide profiling of transcriptomics during the induction of human Th17 differentiation provides a starting point for defining gene regulatory networks and identifying new candidates regulating Th17 differentiation in humans.

scholarly journals Recent progress towards understanding the role of DNA methylation in human placental development

Reproduction ◽  
2016 ◽  
Vol 152 (1) ◽  
pp. R23-R30 ◽  
Author(s):  
Tina Bianco-Miotto ◽  
Benjamin T Mayne ◽  
Sam Buckberry ◽  
James Breen ◽  
Carlos M Rodriguez Lopez ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Pregnancy Complications ◽  
Large Scale ◽  
Developmental Stages ◽  
Epigenetic Modifications ◽  
Placental Development ◽  
Functional Changes ◽  
Genome Wide

Epigenetic modifications, and particularly DNA methylation, have been studied in many tissues, both healthy and diseased, and across numerous developmental stages. The placenta is the only organ that has a transient life of 9 months and undergoes rapid growth and dynamic structural and functional changes across gestation. Additionally, the placenta is unique because although developing within the mother, its genome is identical to that of the foetus. Given these distinctive characteristics, it is not surprising that the epigenetic landscape affecting placental gene expression may be different to that in other healthy tissues. However, the role of epigenetic modifications, and particularly DNA methylation, in placental development remains largely unknown. Of particular interest is the fact that the placenta is the most hypomethylated human tissue and is characterized by the presence of large partially methylated domains (PMDs) containing silenced genes. Moreover, how and why the placenta is hypomethylated and what role DNA methylation plays in regulating placental gene expression across gestation are poorly understood. We review genome-wide DNA methylation studies in the human placenta and highlight that the different cell types that make up the placenta have very different DNA methylation profiles. Summarizing studies on DNA methylation in the placenta and its relationship with pregnancy complications are difficult due to the limited number of studies available for comparison. To understand the key steps in placental development and hence what may be perturbed in pregnancy complications requires large-scale genome-wide DNA methylation studies coupled with transcriptome analyses.

scholarly journals AGL16 regulates genome-wide gene expression and flowering time with partial dependency on SOC1 in Arabidopsis

2021 ◽  
Author(s):  
Xue Dong ◽  
Li-Ping Zhang ◽  
Dongmei Yu ◽  
Fang Cheng ◽  
Yinxin Dong ◽  
...  
Keyword(s):  
Gene Expression ◽  
Flowering Time ◽  
Regulatory Networks ◽  
Binding Property ◽  
Loss Of Function ◽  
Genome Wide ◽  
Carg Box ◽  
Gene Regulatory ◽  
Genome Wide Gene Expression

Flowering transition is pivotal and tightly regulated by complex gene-regulatory-networks, in which AGL16 plays important roles. But the molecular function and binding property of AGL16 is not fully explored in vivo. With ChIP-seq and comparative transcriptomics approaches, we characterized the AGL16 targets spectrum and tested its close molecular and genetic interactions with SOC1, the key flowering integrator. AGL16 bound to promoters of more than 2000 genes via CArG-box motifs that were highly similar to that of SOC1. Being consistent with this, AGL16 formed protein complex and shared a common set of targets with SOC1. However, only very few genes showed differential expression in the agl16-1 loss-of-function mutant, whereas in the soc1-2 knockout background, AGL16 repressed and activated the expression of 375 and 182 genes, respectively, with more than a quarter of the DEGs were also bound by AGL16. AGL16 targeted potentially to about seventy flowering time genes involved in multiple pathways. Corroborating with these, AGL16 repressed the flowering time stronger in soc1-2 than in Col-0 background. These data reveals that AGL16 regulates gene expression and flowering time with a partial dependency on SOC1 activity. Moreover, AGL16 participated in the regulation of water loss and seed dormancy. Our study thus defines the AGL16 molecular spectrum and provides insights underlining the molecular coordination of flowering and environmental adaptation.

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