Search

Early in embryogenesis, maternally deposited transcripts are degraded and new zygotic transcripts are generated during the maternal to zygotic transition. Recent works have shown that early zygotic transcripts are short compared to maternal transcripts, in zebrafish and Drosophila species. The reduced zygotic transcript length was attributed to the short cell cycle in these organisms that prevents the transcription of long primary transcripts (intron delay). Here we study the length of maternal mRNAs and their degradation kinetics in two sea urchin species to further the understanding of maternal gene usage and processing. Early zygotic primary transcripts and mRNAs are shorter than maternal ones in the sea urchin, Strongylocentrotus purpuratus . Yet, while primary transcripts length increases when cell cycle lengthens, typical for intron delay, the relatively short length of zygotic mRNAs is consistent. The enhanced mRNA length is due to significantly longer maternal open reading frames and 3′UTRs compared to the zygotic lengths, a ratio that does not change with developmental time. This implies unique usage of both coding sequences and regulatory information in the maternal stage compared to the zygotic stages. We extracted the half-lifetimes due to maternal and zygotic degradation mechanisms from high-density time course of a set of maternal mRNAs in Paracentrotus lividus . The degradation rates due to maternal and zygotic degradation mechanisms are not correlated, indicating that these mechanisms are independent and relay on different regulatory information. Our studies illuminate specific structural and kinetic properties of sea urchin maternal mRNAs that might be broadly shared by other organisms. [ABSTRACT FROM AUTHOR]

The time required to transcribe genes with long primary transcripts may limit their ability to be expressed in cells with short mitotic cycles, a phenomenon termed intron delay. As such short cycles are a hallmark of the earliest stages of insect development, we tested the impact of intron delay on the Drosophila developmental transcriptome. We find that long zygotically expressed genes show substantial delay in expression relative to their shorter counterparts, which is not observed for maternally deposited transcripts. Patterns of RNA-seq coverage along transcripts show that this delay is consistent with their inability to completely transcribe long transcripts, but not with transcriptional initiation-based regulatory control. We further show that highly expressed zygotic genes maintain compact transcribed regions across the Drosophila phylogeny, allowing conservation of embryonic expression patterns. We propose that the physical constraints of intron delay affect patterns of expression and the evolution of gene structure of a substantial portion of the Drosophila transcriptome. [ABSTRACT FROM PUBLISHER]

Retroposition, a leading mechanism for gene duplication, is an important process shaping the evolution of genomes. Retrogenes are also involved in the gene structure evolution as a major player in the process of intron deletion. Here, we demonstrate the role of retrogenes in intron gain in mammals. We identified one case of “intronization,” the transformation of exonic sequences into an intron, in the primate specific retrogene RNF113B and two independent “intronization” events in the retrogene DCAF12L2, one in the common ancestor of primates and rodents and another one in the rodent lineage. Intron gain resulted from the origin of new splice variants, and both genes have two transcript forms, one with retained intron and one with the intron spliced out. Evolution of these genes, especially RNF113B, has been very dynamic and has been accompanied by several additional events including parental gene loss, secondary retroposition, and exaptation of transposable elements. [ABSTRACT FROM PUBLISHER]

Abstract: Antisense transcripts are widespread phenomenon in eukaryotes. However, protein coding genes overlapping with other protein genes at both, ends are very rare in the human and other vertebrate genomes. Here, we report a comparative analysis of a region in the human chromosome 1 where two neighboring genes overlap with other genes at each end. The aim of this study was to analyze the evolution of this phenomenon and to identify relations, if any, in the expression patterns of the involved genes. We identified orthologs of six genes from the human region 1p34.3–1p34.1, MUTYH, TOE1, TESK2, LOC126661, MMACHC, and PRDX1, in vertebrates, insects, sea urchin, and Arabidopsis genomes and performed detailed analysis of their genomic arrangements. In addition we investigated expression of these genes in humans and mice. Presented data demonstrate that this specific arrangement of six genes is primate specific and involves both, genes conserved in all lineages as well as young, lineage specific genes. The overlap of these genes does not enforce any specific pattern of gene expression and no pair of overlapping genes showed negative correlation in the expression pattern. Additionally, this study shows that overlapping genes tend to have more splice variants then their non-overlapping orthologs and that there is a big dynamics in the gene structure evolution resulting in colossal differences in gene structure in closely related species. [Copyright &y& Elsevier]

Abstract: The exon–intron structure of eukaryotic genes allows for phenomena such as alternative splicing, nonsense-mediated decay, and regulation through untranslated regions. However, the evolution of the exon structure of genes is not well elucidated because of limited and phylogenetically sparse data sets. In this study, we use the phylogenetically diverse sequencing of the ENCODE regions to study gene structure evolution in mammalian genomes. This first phylogenetically diverse study of gene structure changes offers insights into the mode and tempo of mammalian gene structure evolution. The genes undergoing structure changes appear to be moderately to highly expressed in germline cells and show levels of selection similar to those of other ENCODE genes. Patterns of gene duplication of the affected genes are more complex than expected. The number of sampled genomes is sufficiently dense to infer that certain gene duplications happened after intron loss. Thus, although gene duplication is highly correlated with intron loss, we conclude that structural changes in genes are not necessarily due to a loss of constraint following gene duplication as previously suggested. [Copyright &y& Elsevier]