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Tissue-specific activity of the blind mole rat and the two nucleotide-mutated mouse alphaB-crystallin promoter in transgenic mice.

ABSTRACT: The alphaB-crystallin and HspB2 genes are located approximately 0.9 kb apart in a head-to-head arrangement in mammals. Previous experiments have shown that a truncated -668/+45 alphaB-crystallin enhancer/promoter fragment from blind mole rats (Spalax ehrenbergi), which have nonfunctional lenses, lacks lens activity and has enhanced muscle activity in transgenic mice. Here we show that the full-length mole rat alphaB-crystallin intergenic region behaves similarly in transgenic mice. A two-nucleotide mutation ((-273)CA-->G) in the mouse alphaB-crystallin enhancer/promoter fragment mimicking the wild-type mole rat sequence functionally converted the mouse promoter fragment to that of the wild-type mole rat promoter when tested in transgenic mice. The reciprocal mutation in the mole rat promoter fragment ((-272)G-->CA) did not affect its activity. Oligonucleotides from the wild-type mouse and mole rat alphaB-crystallin promoter region under study formed distinct complexes with nuclear proteins from cultured cells. The mouse mutant sequence lost binding ability, whereas the mutated mole rat sequence gained the ability to form a complex similar in size to that of the wild-type mouse oligonucleotide. Our data support the idea that blind mole rats' alphaB-crystallin promoter activity was modified during the evolution of subterranean life and shows that tissue-specific promoter activity can be modulated by changing as few as two apparently neutral nucleotides in the mouse alphaB-crystallin enhancer region, implying the importance of the context of regulatory sequences for promoter activity.

SUBMITTER: Li Y

PROVIDER: S-EPMC1796782 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Sympatric speciation (SS), i.e., speciation within a freely breeding population or in contiguous populations, was first proposed by Darwin [Darwin C (1859) On the Origins of Species by Means of Natural Selection] and is still controversial despite theoretical support [Gavrilets S (2004) Fitness Landscapes and the Origin of Species (MPB-41)] and mounting empirical evidence. Speciation of subterranean mammals generally, including the genus Spalax, was considered hitherto allopatric, whereby new species arise primarily through geographic isolation. Here we show in Spalax a case of genome-wide divergence analysis in mammals, demonstrating that SS in continuous populations, with gene flow, encompasses multiple widespread genomic adaptive complexes, associated with the sharply divergent ecologies. The two abutting soil populations of S. galili in northern Israel habituate the ancestral Senonian chalk population and abutting derivative Plio-Pleistocene basalt population. Population divergence originated ?0.2-0.4 Mya based on both nuclear and mitochondrial genome analyses. Population structure analysis displayed two distinctly divergent clusters of chalk and basalt populations. Natural selection has acted on 300+ genes across the genome, diverging Spalax chalk and basalt soil populations. Gene ontology enrichment analysis highlights strong but differential soil population adaptive complexes: in basalt, sensory perception, musculature, metabolism, and energetics, and in chalk, nutrition and neurogenetics are outstanding. Population differentiation of chemoreceptor genes suggests intersoil population's mate and habitat choice substantiating SS. Importantly, distinctions in protein degradation may also contribute to SS. Natural selection and natural genetic engineering [Shapiro JA (2011) Evolution: A View From the 21st Century] overrule gene flow, evolving divergent ecological adaptive complexes. Sharp ecological divergences abound in nature; therefore, SS appears to be an important mode of speciation as first envisaged by Darwin [Darwin C (1859) On the Origins of Species by Means of Natural Selection].

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Tissue-specific activity of the blind mole rat and the two nucleotide-mutated mouse alphaB-crystallin promoter in transgenic mice.

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