The lasting after-effects of an ancient polyploidy on the genomes of teleosts

Abstract

The ancestor of most teleost fishes underwent a whole-genome duplication event three hundred million years ago. Despite its antiquity, the effects of this event are evident both in the structure of teleost genomes and in how the surviving duplicated genes still operate to drive form and function. I inferred a set of shared syntenic regions that survive from the teleost genome duplication (TGD) using eight teleost genomes and the outgroup gar genome (which lacks the TGD). I then phylogenetically modeled the TGD's resolution via shared and independent gene losses and applied a new simulation-based statistical test for the presence of bias toward the preservation of genes from one parental subgenome. On the basis of that test, I argue that the TGD was likely an allopolyploidy. I find that duplicate genes surviving from this duplication in zebrafish are less likely to function in early embryo development than are genes that have returned to single copy at some point in this species' history. The tissues these ohnologs are expressed in, as well as their biological functions, lend support to recent suggestions that the TGD was the source of a morphological innovation in the structure of the teleost retina. Surviving duplicates also appear less likely to be essential than singletons, despite the fact that their single-copy orthologs in mouse are no less essential than other genes.

Genomic signatures of globally enhanced gene duplicate accumulation in the megadiverse higher Diptera fueling intralocus sexual conflict resolution

“…The relatively high number of underrepresented biological functions could be envisioned to represent functional contexts that are more sensitive to the immediate consequences of gene duplications such as dosage increase. As a point in case, the underrepresentation of developmental functions in the Drosophila population of lineage-specific gene duplicates is consistent with the in most cases highly pleiotropic nature and dosage-sensitive action of developmental regulators, as has been noted in other cases as well (Conant, 2020). And yet, in the comparison between species Drosophila still stands out with a higher number of developmental gene duplicates (Bao et al, 2018), thus documenting a measurable impact of heightened gene duplicate accumulation even on this exceptionally sensitive class of genes.…”

Phylostratic Shift of Whole-Genome Duplications in Normal Mammalian Tissues towards Unicellularity Is Driven by Developmental Bivalent Genes and Reveals a Link to Cancer

“…On one hand, polyploidy is well known as driving gene diversification and speciation in evolution [ 1 ], which is a slow process. On the other hand, its epigenetic effect causing rapid reorganization of the transcriptional regulatory network after genome duplication was shown [ 95 , 96 ].…”

Early, nonlethal ploidy and genome size quantification using confocal microscopy in zebrafish embryos

“…There is no clear consensus for the pattern employed by invertebrates in response to changes in ploidy and cell size but recent discoveries of WGDs in spiders (Schwager et al, 2017) and horseshoe crabs (Kenny et al, 2016) emphasize that the developmental and morphological consequences of WGDs are relevant for invertebrates as well. As we discover more genome duplications events, we are learning about the genetic consequences of polyploidy in animals (Braasch & Postlethwait, 2012; Conant, 2020; Fagernes et al, 2015; Maciak et al, 2015; Mueller, 2015; Otto, 2007; Postlethwait, 2007) but we are lagging behind in understanding how these changes affect development and physiology. Perhaps the evolution of compensatory mechanism(s) that maintain allometric relationships independently of cell size changes were driven by changes in genome size.…”