The amazing coloration shown by diverse cichlid fish not only fascinates aquarium keepers, but also receives great attention from biologists interested in speciation because of its recently-revealed role in their adaptive radiation in an African lake. We review the important role of coloration in the speciation and adaptive evolution of Lake Victoria cichlids, which have experienced adaptive radiation during a very short evolutionary period. Mature male cichlids display their colors during mate choice. The color of their skin reflects light, and the reflected light forms a color signal that is received by the visual system of females. The adaptive divergence of visual perceptions shapes and diverges colorations, to match the adapted visual perceptions. The divergence of visual perception and coloration indicates that the divergence of color signals causes reproductive isolation between species, and this process leads to speciation. Differences in color signals among coexisting species act to maintain reproductive isolation by preventing hybridization. Thus, the diversity of coloration has caused speciation and has maintained species diversity in Lake Victoria cichlids.
The purpose of this article is to provide basic knowledge about the Mc1r-Asip system that promotes the evolution of coat color in mammals, and to stimulate genetic, ecological, and phylogeographic studies focusing on color variation in natural populations. The topics reviewed herein include: the genetic system of the Mc1r and Asip genes related to phenotypic variation; the evolutionary implications of the genetic features recorded in their nucleotide sequences; and the validity of surveys in the wild of genetic variations in coat color, which would facilitate a better understanding of the genetic system, ecological meaning, natural history, and taxonomic reevaluation of species and local populations.
The molecular basis of pigmentation variation within and among Drosophila species is largely attributed to genes in melanin biosynthesis pathway, which involves dopamine metabolism. Most of the genetic changes underlying pigmentation variations reported to date are changes at the expression levels of the structural genes in the pathway. Within D. melanogaster, changes in cis-regulatory regions of a gene, ebony, are responsible for the naturally occurring variation of the body pigmentation intensity. This gene is also known to be expressed in glia, and many visual and behavioral abnormalities of its mutants have been reported. This implies that the gene has pleiotropic functions in the nervous systems. In this review, current knowledge on pigmentation variation and melanin biosynthesis pathway are summarized, with some focus on pleiotropic features of ebony and other genes in the pathway. A potential association between pigmentation and behavior through such pleiotropic genes is discussed in light of cis-regulatory structure and pleiotropic mutations.
E. coli YdbK is predicted to be a pyruvate:flavodoxin oxidoreductase (PFOR). However, enzymatic activity and the regulation of gene expression of it are not well understood. In this study, we found that E. coli cells overexpressing the ydbK gene had enhanced PFOR activity, indicating the product of ydbK to be a PFOR. The PFOR was labile to oxygen. The expression of ydbK was induced by superoxide generators such as methyl viologen (MV) in a SoxS-dependent manner after a lag period. We identified a critical element upstream of ydbK gene required for the induction by MV and proved direct binding of SoxS to the element. E. coli ydbK mutant was highly sensitive to MV, which was enhanced by additional inactivation of fpr gene encoding ferredoxin (flavodoxin):NADP(H) reductase (FPR). Aconitase activity, a superoxide sensor, was more extensively decreased by MV in the E. coli ydbK mutant than in wild-type strain. The induction level of soxS gene was higher in E. coli ydbK fpr double mutant than in wild-type strain. These results indicate that YdbK helps to protect cells from oxidative stress. It is possible that YdbK maintains the cellular redox state together with FPR and is involved in the reduction of oxidized proteins including SoxR in the late stages of the oxidative stress response in E. coli.
Heavy-ion beams are powerful mutagens. They cause a broad spectrum of mutation phenotypes with high efficiency even at low irradiation doses and short irradiation times. These mutagenic effects are due to dense ionisation in a localised region along the ion particle path. Linear energy transfer (LET; keV·μm–1), which represents the degree of locally deposited energy, is an important parameter in heavy-ion mutagenesis. For high LET radiation above 290 keV∙μm–1, however, neither the mutation frequency nor the molecular nature of the mutations has been fully characterised. In this study, we investigated the effect of Fe-ion beams with an LET of 640 keV∙μm–1 on both the mutation frequency and the molecular nature of the mutations. Screening of well-characterised mutants (hy and gl) revealed that the mutation frequency was lower than any other ion species with low LET. We investigated the resulting mutations in the 4 identified mutants. Three mutants were examined by employing PCR-based methods, one of which had 2-bp deletion, another had 178 bp of tandemly duplication, and other one had complicated chromosomal rearrangements with variable deletions in size at breakpoints. We also detected large deletions in the other mutant by using array comparative genomic hybridisation. From the results of the analysis of the breakpoints and junctions of the detected deletions, it was revealed that the mutants harboured chromosomal rearrangements in their genomes. These results indicate that Fe-ion irradiation tends to cause complex mutations with low efficiency. We conclude that Fe-ion irradiation could be useful for inducing chromosomal rearrangements or large deletions.
Identifying susceptible genes associated with the pathogenesis of atherosclerosis (ATH) may contribute toward better management of this condition. This preliminary study was aimed at assessing the expression levels of 11 candidate genes, namely tumor protein (TP53), transforming growth factor, beta receptor II (TGFBR2), cysthathionenine-beta-synthase (CBS), insulin receptor substrate 1 (IRS1), lipoprotein lipase (LPL), methylenetetrahydrofolate reductase (MTHFR), thrombomodulin (THBD), lecithin-cholesterol acyltransferase (LCAT), matrix metallopeptidase 9 (MMP9), low density lipoprotein receptor (LDLR), and arachidonate 5-lipoxygenase-activating protein (ALOX5AP) genes associated with ATH. Twelve human coronary artery tissues (HCATs) were obtained from deceased subjects who underwent post-mortem procedures. Six atherosclerotic coronary artery tissue (ACAT) samples representing the cases and non-atherosclerotic coronary artery tissue (NCAT) samples as controls were gathered based on predetermined inclusion and exclusion criteria. Gene expression levels were assessed using the GenomeLab Genetic Analysis System (GeXP). The results showed that LDLR, TP53, and MMP9 expression levels were significantly increased in ACAT compared to NCAT samples (p < 0.05). Thus, LDLR, TP53, and MMP9 genes may play important roles in the development of ATH in a Malaysian study population.
Asian and non-Asian populations have been reported to differ substantially in the distribution of fragile X alleles into the normal (< 55 CGG repeats), premutation (55–199 CGG repeats), and full-mutation (> 199 CGG repeats) size classes. Our statistical analyses of data from published general-population studies confirm that Asian populations have markedly lower frequencies of premutation alleles, reminiscent of earlier findings for expanded alleles at the Huntington’s Disease locus. To examine historical and contemporary factors that may have shaped and now sustain allele-frequency differences at the fragile X locus, we develop a population-genetic/epigenetic model, and apply it to these published data. We find that founder-haplotype effects likely contribute to observed frequency differences via substantially lower mutation rates in Asian populations. By contrast, any premutation frequency differences present in founder populations would have disappeared in the several millennia since initial establishment of these groups. Differences in the reproductive fitness of female premutation carriers arising from fragile X primary ovarian insufficiency (FXPOI) and from differences in mean maternal age may also contribute to global variation in carrier frequencies.