Follow titles, links and abstracts of three
open access genetic papers that I feel are interesting enough to mention but are too technical and distant from my main focus to be discussed meaningfully here:
What is a species? The example of lemurs
Matthias Markoff et al., On species delimitation: Yet another lemur species or just genetic variation? BMC Evolutionary Biology 2011. [LINK]
Abstract (provisional)
Background
Although most taxonomists agree that species are independently evolving metapopulation lineages that should be delimited with several kinds of data, the taxonomic practice in Malagasy primates (Lemuriformes) looks quite different. Several recently described lemurs are based solely on evidence of genetic distance and diagnostic characters of mitochondrial DNA sequences sampled from a few individuals per location. Here we explore the validity of this procedure for species delimitation in lemurs using published sequence data.
Results
We show that genetic distance estimates and Population Aggregation Analysis (PAA) are inappropriate for species delimitation in this group of primates. Intra- and interspecific genetic distances overlapped in 14 of 17 cases independent of the genetic marker used. A simulation of a fictive taxonomic study indicated that for the mitochondrial D-loop the minimum required number of individuals sampled per location is 10 in order to avoid false positives via PAA.
Conclusions
Genetic distances estimates and PAA alone should not be used for species delimitation in lemurs. Instead, several nuclear and sex-specific loci should be considered and combined with other data sets from morphology, ecology or behavior. Independent of the data source, sampling should be done in a way to ensure a quantitative comparison of intra- and interspecific variation of the taxa in question. The results of our study also indicate that several of the recently described lemur species should be reevaluated with additional data and that the number of good species among the currently known taxa is probably lower than currently assumed.
Horizontally acquired genes: breaching the gate is not getting the treasure automatically, you may also end in the dungeons
H. Deborah Chen et al., Ancestral Genes Can Control the Ability of Horizontally Acquired Loci to Confer New Traits. PLoS Genetics 2011. [LINK]
Abstract
Horizontally acquired genes typically function as autonomous units conferring new abilities when introduced into different species. However, we reasoned that proteins preexisting in an organism might constrain the functionality of a horizontally acquired gene product if it operates on an ancestral pathway. Here, we determine how the horizontally acquired pmrD gene product activates the ancestral PmrA/PmrB two-component system in Salmonella enterica but not in the closely related bacterium Escherichia coli. The Salmonella PmrD protein binds to the phosphorylated PmrA protein (PmrA-P), protecting it from dephosphorylation by the PmrB protein. This results in transcription of PmrA-dependent genes, including those conferring polymyxin B resistance. We now report that the E. coli PmrD protein can activate the PmrA/PmrB system in Salmonella even though it cannot do it in E. coli, suggesting that these two species differ in an additional component controlling PmrA-P levels. We establish that the E. coli PmrB displays higher phosphatase activity towards PmrA-P than the Salmonella PmrB, and we identified a PmrB subdomain responsible for this property. Replacement of the E. coli pmrB gene with the Salmonella homolog was sufficient to render E. coli resistant to polymyxin B under PmrD-inducing conditions. Our findings provide a singular example whereby quantitative differences in the biochemical activities of orthologous ancestral proteins dictate the ability of a horizontally acquired gene product to confer species-specific traits. And they suggest that horizontally acquired genes can potentiate selection at ancestral loci.
Author Summary
The traits that distinguish closely related bacterial species are often ascribed to differences in gene content, which arise primarily through horizontal gene transfer. In some instances, the genes mediating a new trait act as independent entities that function in a variety of organisms. However, the ability of a horizontally acquired gene product(s) to operate on an ancestral pathway might be constrained by subtle differences between orthologous ancestral proteins. Here, we examine why the horizontally acquired pmrD gene product post-translationally activates the ancestral PmrA/PmrB two-component system in Salmonella enterica but not in the closely related species Escherichia coli. This allows Salmonella, but not E. coli, to transcribe PmrA-activated genes including those conferring antibiotic resistance when grown in low Mg2+, which is a condition that promotes PmrD expression. We now demonstrate that, paradoxically, the E. coli PmrD protein activates the PmrA/PmrB system in Salmonella even though it fails to do so in E. coli. We establish that quantitative differences in the biochemical activities of the PmrB proteins from Salmonella and E. coli dictate the functionality of PmrD, which protects phosphorylated PmrA from PmrB's phosphatase activity. Our findings demonstrate that ancestral genes can control the ability of horizontally acquired genes to confer species-specific traits upon different organisms.
Day and night cycle in our cells, the clock inside us and its epigenetic synchronization
William J. Belden et al., CHD1 Remodels Chromatin and Influences Transient DNA Methylation at the Clock Gene frequency. PLoS Genetics 2011. [LINK]
Abstract
Circadian-regulated gene expression is predominantly controlled by a transcriptional negative feedback loop, and it is evident that chromatin modifications and chromatin remodeling are integral to this process in eukaryotes. We previously determined that multiple ATP–dependent chromatin-remodeling enzymes function at frequency (frq). In this report, we demonstrate that the Neurospora homologue of chd1 is required for normal remodeling of chromatin at frq and is required for normal frq expression and sustained rhythmicity. Surprisingly, our studies of CHD1 also revealed that DNA sequences within the frq promoter are methylated, and deletion of chd1 results in expansion of this methylated domain. DNA methylation of the frq locus is altered in strains bearing mutations in a variety of circadian clock genes, including frq, frh, wc-1, and the gene encoding the frq antisense transcript (qrf). Furthermore, frq methylation depends on the DNA methyltransferase, DIM-2. Phenotypic characterization of Δdim-2 strains revealed an approximate WT period length and a phase advance of approximately 2 hours, indicating that methylation plays only an ancillary role in clock-regulated gene expression. This suggests that DNA methylation, like the antisense transcript, is necessary to establish proper clock phasing but does not control overt rhythmicity. These data demonstrate that the epigenetic state of clock genes is dependent on normal regulation of clock components.
Author Summary
Circadian rhythms facilitate daily changes in gene expression via a transcriptional negative feedback loop. In eukaryotes, chromatin remodeling is an integral part of transcriptional regulation and is proving to be one of the major determinants for the proper timing and amplitude of clock-gene expression. We describe here the action of chromodomain helicase DNA–binding (CHD1), one of two ATP–dependent chromatin-remodeling enzymes required for normal circadian regulated gene expression of the central clock gene frequency (frq). Molecular analysis of strains lacking chd1 indicates that CHD1 is required for remodeling chromatin structure at the frq locus as a part of the daily clock cycle. Moreover, we discovered DNA methylation in the promoter of frq that diminishes over time in the absence of light/dark cycles and determined that normal DNA methylation appears to require a functional clock. The DNA methyltransferase DIM-2 is responsible for this DNA methylation, and the DNA methylation is required for proper phasing of clock gene expression. Collectively, these data demonstrate a close connection among chromatin remodeling, DNA methylation, and clock gene expression.
