The zebrafish genome in context: ohnologs gone missing

Abstract

Some zebrafish genes appear to lack an ortholog in the human genome and researchers often call them ''novel'' genes. The origin of many so-called ''novel'' genes becomes apparent when considered in the context of genome duplication events that occurred during evolution of the phylum Chordata, including two rounds at about the origin of the subphylum Vertebrata (R1 and R2) and one round before the teleost radiation (R3). Ohnologs are paralogs stemming from such genome duplication events, and some zebrafish genes said to be ''novel'' are more appropriately interpreted as ''ohnologs gone missing'', cases in which ohnologs are preserved differentially in different evolutionary lineages. Here we consider ohnologs present in the zebrafish genome but absent from the human genome. Reasonable hypotheses are that lineage-specific loss of ohnologs can play a role in establishing lineage divergence and in the origin of developmental innovations. How does the evolution of ohnologs differ from the evolution of gene duplicates arising from other mechanisms, such as tandem duplication or retrotransposition? To what extent do different major vertebrate lineages or different teleost lineages differ in ohnolog content? What roles do differences in ohnolog content play in the origin of developmental mechanisms that differ among lineages? This review explores these questions.

Characterization of the neuroligin gene family expression and evolution in zebrafish

“…Taken together, phylogenetic and syntenic analyses confirm that all the zebrafish Neuroligin genes derived from a whole genome duplication event occurred at the base of the teleost radiation at approximately 350 Mya (Postlethwait, 2007). Both paralogous genes survived during evolution with the exception of one duplicate of Neuroligin 1, which has been lost before the first speciation events within the teleosts.…”

“…In zebrafish, Neuroligin 2-4 genes are duplicated; only the Neuroligin 1 gene seems to be present in a single copy and, notwithstanding extensive database searches, we did not find any traces of a duplicate form of this gene. The lack of a Neuroligin 1 paralogous gene in other teleosts such as G. aculeatus, O. latipes, T. nigrovirids, and T. rubripes (see below) strongly suggests that, after the whole genome duplication (Postlethwait, 2007), one copy quickly disappeared.…”

“…Because of functional redundancy, most new gene copies tend to accumulate deleterious mutations and degenerate into pseudogenes before being, eventually, lost (Ohno, 1970(Ohno, , 1973Holland et al, 1994;Sidow, 1996;Petrov and Hartl, 2000;Postlethwait, 2007). Alternative fates of duplicated genes are neofunctionalization and subfunctionalization.…”

“…Alternative fates of duplicated genes are neofunctionalization and subfunctionalization. In neofunctionalization, one or both paralogous genes acquire new functional roles; in subfunctionalization, the genes divide their original functions (Postlethwait et al, 2004;Taylor and Raes, 2004;Postlethwait, 2007). In addition to gene duplication, alternative splicing is another major source of protein function diversity.…”

Automated identification of conserved synteny after whole-genome duplication

“…Events such as gene duplications or whole genome duplications (WGD), with associated differential gene loss, introduce noise into these analyses. Anomalies, such as lineage-specific paralog loss, can cause anciently related homologs to appear to be orthologs, thereby confusing sequence similarity with functional homology (Postlethwait 2007). Such errors can confound attempts to create nonhuman animal disease models and can obscure recent, speciesspecific evolutionary change among sister lineages.…”