The eutherian genome has presumably undergone two rounds of whole genome duplication (2R Hypothesis) occurring in early chordate evolution (Urochordata–Craniata) ( Garcia-Fernandez and Holland 1994 Dehal and Boore 2005 Hallbook et al. The molecular evolution of a protein family involves a combination of gene expansion events that includes gene duplication and duplication of the whole genome ( Haldane 1932 Ohno 1970, 1993 Taylor and Raes 2004 Domazet-Loso et al. We were able to identify that within the highly conserved meEM motif two regions, which are unique to all therian species, appear to be the most derived features in the SLC26A5 peptide. Clade-specific substitutions were not observed and there was no sequence correlation with low or high hearing frequency specialists. Within the eutherian clade, the meEM was highly conserved with a substitution frequency of only 39/7497 (0.5%) residues, compared with 5.7% in SLC26A4 and 12.8% in SLC26A6 genes. Suggested from the point-accepted mutation analysis, the meEM motif spans all the transmembrane segments and represented residues 66–503. The opossum and platypus SLC26A5 proteins were comparable to the eutherian consensus sequence. Comparisons were done among nonmammalian vertebrates, eutherian mammalian species, and the opossum and platypus. A putative minimal essential motif for the electromotility motor (meEM) was identified through the amalgamation of comparative genomic, evolution, and structural diversification approaches. The ion transporter capability, typical of SLC26A members, was exchanged for electromotility function and is a newly derived feature of the therian cochlea. PLoS Biol, 6(3), e63.Prestin (SLC26A5) is the molecular motor responsible for cochlear amplification by mammalian cochlea outer hair cells and has the unique combined properties of energy-independent motility, voltage sensitivity, and speed of cellular shape change. Loss of egg yolk genes in mammals and the origin of lactation and placentation. Why do mammals that do not lay eggs have non-functional egg yolk genes in their genomes? If these species do not lay eggs and didn’t evolve from ancestors that lay eggs, why would God have put these in their genomes? Why do some mammals share some identical loss-of-function mutations in their egg yolk genes genes?ġ. Together, these data suggest that the inactivation of egg yolk genes in placental and marsupial mammals is connected with the loss of their egg-laying ability through evolutionary time. Gallus gallus = chicken Monodelphis domestica = opossum Macropus eugenii and Wallabia bicolor = wallabies.īy contrast, at least one egg yolk gene is intact in the egg-laying platypus. Highlighted portions indicate loss-of-function mutations. DNA sequence alignment of egg-yolk genes. Similarly, the researchers found remnants of three egg-yolk genes ( VIT1, VIT2, VIT3) in the marsupials they studied (opossum, wallabies), with shared loss-of-function mutations in each (Figure 1), which, again, imply loss in a common ancestor.įigure 1. These mammals share some loss-of-function mutations in the genes, suggesting that the genes were inactivated in a common ancestor.
So how might one test this hypothesis? David Brawand and his colleagues had the idea of looking at the genomes of mammals to see if they have any remnants of egg yolk genes.īesides monotremes, the remaining mammals can be divided into two general groups: (1) marsupials, whose offspring are born early in development and then finish developing in a pouch (marsupium), and (2) placental mammals, which develop with the help of a placenta connecting the mother to the fetus. When Brawand and his colleagues looked at the genomes of three placental mammals (human, dog, armadillo), they found remnants of two egg-yolk genes ( VIT1, VIT3), both of which possessed loss-of-function mutations.
#Platypus evolution meta plus
The fact that a few mammals lay eggs, plus that most other land-dwelling vertebrates do as well, points to the idea that the rest of mammals descended from egg-layers.
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