Ψ ARR3 - Hipposideros armiger
Reference Gene:
Job_ID:
Curator:
| GlossID | Species | Gene Loss Mechanism | Loss Type | Lineage Specific | Evidence | Accession Nr. |
|---|---|---|---|---|---|---|
| GL_BOMBFN | Hipposideros armiger | LOF (frameshift, premature stop, ss) | Full | No | Genomic | XM_019647973.1 |
Statements
| Type | Excerpt | DOI |
|---|---|---|
| Functional | "eye-enriched visual perception genes" | 10.1093/icb/icy004 |
| Methodology & Validation | "I obtained human curated mRNA reference sequences (accession prefix “NM_”) from NCBI’s nucleotide collection (Supplementary Table S1), and BLASTed (discontiguous megablast) the entire set of genes against the nucleotide collection for each of the remaining 29 mammals. For every species, I obtained gene models derived from NCBI’s Eukaryotic Genome Annotation (EGA) pipeline (accession prefix “XM_”) and/or curated mRNAs.[…] Curated mRNAs were assumed to encode functional protein products, as were gene models, unless there was an annotation indicating the gene likely encodes a “low quality protein”.[…] considered predicted pseudogenes with two or more corrected frameshifts and/or premature stop codons to be “probable pseudogenes” […]." | 10.1093/icb/icy004 |
| Other | "Numerous other genes associated with visual functions, such as ARR3 (cone arrestin), CRB1 (crumbs homolog 1 [Drosophila]), GRK7 (G proteincoupled receptor kinase 7), GUCA1B (guanylate cyclase activator 1B), and GUCY2F (guanylate cyclase 2F, retinal) have been inactivated in various mammals (Emerling and Springer 2014; Hudson et al. 2014), particularly nocturnal species, and multiple genes involved in cone phototransduction have been pseudogenized in several whale lineages (Meredith et al., 2013; Emerling and Springer, 2015; Springer et al., 2016)." | 10.1093/icb/icy004 |
Curator Observations
Only “probable pseudogenes” defined as genes tagged with “low quality protein” containing multiple inactivating mutations and genes with absent BLAST results were collected from this publication, following the authors assumption “that a gene with multiple putative inactivating mutations is less likely to results from unfixed variants or sequencing or assembly errors”.