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We sequenced the mitochondrial genome of the Western green lizard (Lacerta bilineata) using Illumina technology and additional Sanger sequencing. The assembled 17 086 bp mitogenome had a GC content of 40.32% and consisted of 13 protein-coding genes, 22 tRNA genes, two rRNA genes, and one control region (CR), with a gene order identical to the chordate consensus. In addition, we re-sequenced the mitogenome of the closely related Eastern green lizardL. viridisusing the same techniques as forL. bilineata. The mitogenomes ofL. bilineataandL. viridisshowed a sequence identity of 94.4% and 99.9%, respectively, relative to the previously publishedL. viridismitogenome. The phylogenetic reconstruction based on 17 Lacertinae mitogenomes usingAnolis carolinensisas the outgroup supportedL. bilineataand its sister speciesL. viridisas distinct lineages. [ABSTRACT FROM PUBLISHER]

The comprehensive understanding of mitochondrial genome evolution requires a detailed mechanistic picture of mitogenomic replication. Despite many previous efforts it has remained a non-trivial problem to determine the origins of replication and trace their fate across rearrangements of the gene order even in the small genomes of animal mitochondria. We elaborate here on the observation that the GC skew is correlated with the distance from the replication origins. This effect has been explained as a consequence of the standard model of mitochondrial DNA replication, i.e. the strand displacement model. According to this model chemical damage accumulates proportional to the duration that DNA is exposed in single-stranded form during replication (Dssh) which depends on the relative position with respect to the replication origins. Based on this model we developed a computational method to infer the positions of both the heavy strand and the light strand origin from nucleotide skew data. In a comprehensive survey of deuterostome mitochondria we infer conserved replication origins for the vast majority of vertebrates and cephalochordates. Deviations from the consensus picture are presumably associated with genome rearrangements. [ABSTRACT FROM AUTHOR]

The article presents solutions for transformability of formulas of language L2ω into formulas of language of яω. It presents formulas of language L2ω (FL2ω) to solve for formulas of language L2ω into formulas of language of яω. It defines an algorithm γω to solve for formulas of language L2ω into formulas of language of L2ω.

The article presents solutions for transformability of formulas of language L2ω into formulas of language of яω. It presents formulas of language L2ω (FL2ω) to solve for formulas of language L2ω into formulas of language of яω. It defines an algorithm γω to solve for formulas of language L2ω into formulas of language of L2ω.

Mitochondrial genome sequences are available in large number and new sequences become published nowadays with increasing pace. Fast, automatic, consistent, and high quality annotations are a prerequisite for downstream analyses. Therefore, we present an automated pipeline for fast de novo annotation of mitochondrial protein-coding genes. The annotation is based on enhanced phylogeny-aware hidden Markov models (HMMs). The pipeline builds taxon-specific enhanced multiple sequence alignments (MSA) of already annotated sequences and corresponding HMMs using an approximation of the phylogeny. The MSAs are enhanced by fixing unannotated frameshifts, purging of wrong sequences, and removal of non-conserved columns from both ends. A comparison with reference annotations highlights the high quality of the results. The frameshift correction method predicts a large number of frameshifts, many of which are unknown. A detailed analysis of the frameshifts in nad3 of the Archosauria-Testudines group has been conducted. [ABSTRACT FROM AUTHOR]

Summary A functional crosstalk between epigenetic regulators and metabolic control could provide a mechanism to adapt cellular responses to environmental cues. We report that the well-known nuclear MYST family acetyl transferase MOF and a subset of its non-specific lethal complex partners reside in mitochondria. MOF regulates oxidative phosphorylation by controlling expression of respiratory genes from both nuclear and mtDNA in aerobically respiring cells. MOF binds mtDNA, and this binding is dependent on KANSL3. The mitochondrial pool of MOF, but not a catalytically deficient mutant, rescues respiratory and mtDNA transcriptional defects triggered by the absence of MOF. Mof conditional knockout has catastrophic consequences for tissues with high-energy consumption, triggering hypertrophic cardiomyopathy and cardiac failure in murine hearts; cardiomyocytes show severe mitochondrial degeneration and deregulation of mitochondrial nutrient metabolism and oxidative phosphorylation pathways. Thus, MOF is a dual-transcriptional regulator of nuclear and mitochondrial genomes connecting epigenetics and metabolism. [ABSTRACT FROM AUTHOR]