Transcription and epigenetic regulation of eukaryotes. (A) Promoter structure, polymerase recruitment, initial transcribing complex, and final transcriptional products of Pol I, Pol II, and Pol III. In the promoter structure, known cis-regulatory elements and TFBSs are marked with rectangles. The arrows denote the transcription start sites of transcribing genes. The histones of nucleosomes are indicated with gray circles. In polymerase recruitment, initiation factors (including cofactors, general TFs, and polymerase) are recruited onto promoter regions to form the initially transcribing complex. For the final transcriptional products of Pol III, the promoter type of each transcriptional product is marked in parentheses. (B) The model of closed and open chromatin and their related epigenetic regulation. The compaction of nucleosomes is caused by repressive histone modification and a high level of DNA methylation. During nucleosome decompaction, histone-modifying enzymes (HME) are used to remove repressive histone modification and increase activating histone marks. Remodelers and pioneer TFs are recruited to genes and their upstream regions to remove nucleosomes. In gene silencing, plants use the RdDM pathway to increase DNA methylation. The biological processes of the RdDM pathway require Pol II, Pol III, siRNA, AGO4/6/0, IGN RNAs, and DRM2. UCE, upstream control element. rInr, ribosomal initiator. UAF, upstream activation factor. Pol, polymerase. rRNA, ribosomal RNA. Inr, initiator. mRNA, messenger RNA. tRNA, transfer RNA. snRNA, small nuclear RNA. HME, histone-modifying enzymes. TF, transcription factor. siRNA, small interfering RNA. RdDM, RNA-directed DNA methylation. DRM2, domains rearranged methyltransferase 2. AGO, argonaute protein. IGN RNA, intergenic non-coding RNAs.

Transcription and epigenetic regulation of eukaryotes. (A) Promoter structure, polymerase recruitment, initial transcribing complex, and final transcriptional products of Pol I, Pol II, and Pol III. In the promoter structure, known cis-regulatory elements and TFBSs are marked with rectangles. The arrows denote the transcription start sites of transcribing genes. The histones of nucleosomes are indicated with gray circles. In polymerase recruitment, initiation factors (including cofactors, general TFs, and polymerase) are recruited onto promoter regions to form the initially transcribing complex. For the final transcriptional products of Pol III, the promoter type of each transcriptional product is marked in parentheses. (B) The model of closed and open chromatin and their related epigenetic regulation. The compaction of nucleosomes is caused by repressive histone modification and a high level of DNA methylation. During nucleosome decompaction, histone-modifying enzymes (HME) are used to remove repressive histone modification and increase activating histone marks. Remodelers and pioneer TFs are recruited to genes and their upstream regions to remove nucleosomes. In gene silencing, plants use the RdDM pathway to increase DNA methylation. The biological processes of the RdDM pathway require Pol II, Pol III, siRNA, AGO4/6/0, IGN RNAs, and DRM2. UCE, upstream control element. rInr, ribosomal initiator. UAF, upstream activation factor. Pol, polymerase. rRNA, ribosomal RNA. Inr, initiator. mRNA, messenger RNA. tRNA, transfer RNA. snRNA, small nuclear RNA. HME, histone-modifying enzymes. TF, transcription factor. siRNA, small interfering RNA. RdDM, RNA-directed DNA methylation. DRM2, domains rearranged methyltransferase 2. AGO, argonaute protein. IGN RNA, intergenic non-coding RNAs.

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In eukaryotes, dynamic regulation enables DNA polymerases to catalyze a variety of RNA products in spatial and temporal patterns. Dynamic gene expression is regulated by transcription factors (TFs) and epigenetics (DNA methylation and histone modification). The applications of biochemical technology and high-throughput sequencing enhance the unders...

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Context 1
... transcription initiation, three universal polymerases are recruited by distinct cofactors and transcription factors (TFs) to core promoter regions (Fig. 1A). The cis-regulatory elements (TF binding sites; TFBSs) on promoters enable promoters to have various properties and serve various functions. During the transcription initiation of Pol I, the upstream control element (UCE) must be bound by upstream activating factor (UAF) [3]. Pol II uses diverse and complex cis-regulatory elements to ...
Context 2
... to cis-regulatory elements. Thus, before polymerase recruitment, promoter regions must decompact nucleosomes and remove histones to form open chromatin which serves as a docking site for regulatory proteins [3]. The compaction of nucleosomes can be mediated by DNA methylation of cytosine and posttranslational modifications of histone tails (Fig. 1B); this process is called epigenetic regulation. Epigenetic regulation controls transcription efficiency without altering the DNA sequence. Some changes in epigenome are observed to be inherited by offspring, which helps them to remember stresses from their parents and regulate cell differentiation during development [10][11][12]. Both ...

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Gene expression has a key role in reproductive isolation, and studies of hybrid gene expression have identified mechanisms causing hybrid sterility. Here, we review the evidence for altered gene expression following hybridization and outline the mechanisms shown to contribute to altered gene expression in hybrids. Transgressive gene expression, transcending that of both parental species, is pervasive in early generation sterile hybrids, but also frequently observed in viable, fertile hybrids. We highlight studies showing that hybridization can result in transgressive gene expression, also in established hybrid lineages or species. Such extreme patterns of gene expression in stabilized hybrid taxa suggest that altered hybrid gene expression may result in hybridization‐derived evolutionary novelty. We also conclude that while patterns of misexpression in hybrids are well documented, the understanding of the mechanisms causing misexpression is lagging. We argue that jointly assessing differences in cell composition and cell‐specific changes in gene expression in hybrids, in addition to assessing changes in chromatin and methylation, will significantly advance our understanding of the basis of altered gene expression. Moreover, uncovering to what extent evolution of gene expression results in altered expression for individual genes, or entire networks of genes, will advance our understanding of how selection moulds gene expression. Finally, we argue that jointly studying the dual roles of altered hybrid gene expression, serving both as a mechanism for reproductive isolation and as a substrate for hybrid ecological adaptation, will lead to significant advances in our understanding of the evolution of gene expression.