Dataset Information

Differential transcript isoform usage pre- and post-zygotic genome activation in zebrafish

ABSTRACT: Zebrafish embryos are transcriptional silent until activation of the zygotic genome during the 10th cell cycle. Onset of transcription is followed by cellular and morphological changes involving cell speciation and gastrulation. Previous genome-wide surveys of transcriptional changes only assessed gene expression levels; however, recent studies have shown the necessity to map isoform-specific transcriptional changes. Here we perform isoform discovery and quantification on transcriptome sequences from before and after zebrafish zygotic genome activation (ZGA). We identify novel isoforms and isoform switches during ZGA for genes related to cell adhesion, pluripotency and DNA methylation. Isoform switching events include alternative splicing and changes in transcriptional start sites and in 3’ untranslated regions. New isoforms are identified even for well-characterized genes such as pou5f1, sall4 and dnmt1. Genes involved in cell-cell interactions such as f11r and magi1 display isoform switches with alterations of coding sequences. We also detect over 1000 transcripts that acquire a longer 3’ terminal exon when transcribed zygotically relative to the maternal transcript counterparts. ChIP-seq data mapped onto skipped exon events reveals a correlation between histone H3K36trimethylation peaks and the skipped exons, suggesting epigenetic marks being part of alternative splicing regulation. The novel isoforms and isoform switches reported here include regulators of the transcriptional, cellular and morphological changes taking place around ZGA. Our data display an array of isoform-related functional changes and represent a valuable resource complementary to existing early embryo transcriptomes.

ORGANISM(S): Danio rerio

PROVIDER: GSE40629 | GEO | 2012/11/01

SECONDARY ACCESSION(S): PRJNA174427

REPOSITORIES: GEO

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Project description:The loss of the tail is one of the main anatomical evolutionary changes to have occurred along the lineage leading to humans and to the “anthropomorphous apes”. This morphological evolution in the ancestral hominoids has long been considered to have accommodated a characteristic style of locomotion and contributed to the evolution of bipedalism in humans. Yet, the genetic mechanism that facilitated tail-loss evolution in hominoids remains unknown. Primate genome sequencing projects have made possible the inference of causal links between genotypic and phenotypic changes, and enabled the search for hominoid-specific genetic elements controlling tail development. Here, we present evidence that an individual Alu element insertion in the genome of the hominoid ancestor may have contributed to tail-loss evolution. We demonstrate that this Alu element – inserted into an intron of the TBXT gene (also called T or Brachyury ) – pairs with a neighboring ancestral Alu element encoded in the reverse genomic orientation and leads to a hominoid-specific alternative splicing event. To study the effect of this splicing event, we generated multiple mouse models that express both full length and exon-skipped isoforms of mouse Tbxt, mimicking expression pattern of its hominoid ortholog TBXT. We found that mice expressing both Tbxt isoforms can exhibit a complete absence of the tail or a shortened tail, depending on the relative abundance of Tbxt isoforms expressed at the embryonic tail bud, supporting the notion that the exon-skipped transcript is sufficient to induce a tail-loss phenotype. We further noted that mice expressing the exon-skipped Tbxt isoform – both in heterozygous and homozygous forms – may develop a neural tube defect condition, which affects ~1/1,000 human neonates. We speculate that tail loss evolution along the hominoid lineage may be associated with an adaptive cost of potential neural tube defects that may continue to affect human health today.

Dataset Information

Differential transcript isoform usage pre- and post-zygotic genome activation in zebrafish

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