| Functional |
"AMPD3 encodes an enzyme that deaminates adenosine monophosphate (AMP) to inosine monophosphate (IMP)" "The right shift of the oxygen–hemoglobin dissociation curve observed in AMPD3 knockout mice is likely adaptive for a mammal with long diving times." |
10.1038/s41467-018-03667-1 |
| Methodology & Validation |
"For a gene to be classified as lost, we require that a lineage, which descends from an ancestor with an intact gene, exhibits several gene-inactivating mutations that most likely result in a non-functional protein. As gene-inactivating mutations, we consider frameshifting insertions and deletions, inframe stop codon mutations, and splice site-disrupting mutations. In addition, we consider the loss of exons or even entire genes, which could occur due to either large deletions in the genome or the accumulation of numerous mutations that destroy any sequence similarity. For all previously unknown gene losses presented here, we further confirmed the loss by validating the gene-inactivating mutations with unassembled sequencing reads from the respective species." |
10.1038/s41467-018-03667-1 |
| Timing of Loss |
"Sup Table 5: 31 -37 Million years ago" |
10.1038/s41467-018-03667-1 |
| Phenotypic |
"The function of AMPD3 as a key regulator of the adenine nucleotide pool size in erythrocytes is evident from AMPD3 knockout mice that are phenotypically normal but have a 3 fold higher level of ADP and ATP in erythrocytes." |
10.1038/s41467-018-03667-1 |