Analysis of the locomotor activity of a nocturnal desert lizard (Reptilia: Gekkonidae: Teratoscincus scincus) under varying moonlight

Annals of the New York Academy of Sciences

2019

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Phyloproteomics indicate common viral origin from ancient cells before archaea, bacteria, and eukaryota split and subsequent size and complexity reductions occurred. Further independent evidence for the cellular origin of viruses is reviewed for the virus order Megavirales, focusing on the family Poxviridae. Megavirales comprises giant viruses, double‐stranded DNA viruses whose genomes exceed some bacterial ones and large enough to parasitize large‐celled protists (amoeba). Giant viruses, virophages, and mitochondria have homologous DNA and RNA polymerases and share RNA splicing punctuation by stem–loop hairpins. Giant virus factories and amoeban mitochondria colocate, with viral proteins homologous to mitochondrial proteins specifically targeting mitochondrial inner membranes. Mitochondria share asexual budding with many bacterial endospores and membrane‐enveloped viruses. These megavirus−mitochondrion similarities are not coincidental: systematic alignment analyses have detected candidate megaviral homologs of each amoeban mitogene (including ribosomal RNAs) distributed across megaviral genomes. These candidate megaviral homologs overall follow mitogene order, and megaviral−mitogenome synteny increases with viral genome reduction. This analysis is repeated within Poxviridae, whose organellar‐like morphogenesis is reminiscent of mitochondria. More generally, the results confirm the patterns observed in Megavirales: synteny with amoeban mitogenomes increases with genome reduction. Parsimoniously interpreting this suggests Megavirales and mitochondria have a rickettsia‐like common ancestor. Megavirales could be the missing links between bacterial‐like cells and mitochondria, implying cellular‐to‐viral‐to‐subcellular macroevolution.

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Giant viruses: spore‐like missing links between Rickettsia and mitochondria?

Annals of the New York Academy of Sciences

2019

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“…For each codon family investigated, the percent of polymorphisms that are associated with pathologies was calculated from the two last columns of Table 1 , assuming that this percentage indicates selection on synonymous mutations in that codon family. Because gradient strengths are calculated on different numbers of data (column 3 in Table 1 ), and that sample sizes affect estimates of Pearson correlation coefficients r, these r values which estimate gradient strengths were z transformed using the adjustment method of r for sample size effects used in [48]: z(adjusted)=z - r/(2n-5), where z is the regular z transformation of r, z = log((1+r)/(1-r)) and n is the sample size. For codon pairs with G-A at 3rd position, corresponding to heavy strand deamination gradients of C->T, strengths of z-adjusted replicational and transcriptional gradients (data from Table 1 ) decrease with percentages of pathogenic mutations found for that codon family (r = -0.590 and r =-0.592, respectively, see Fig.…”

Section: Deamination Gradients and Pathogenic Mutationsmentioning

confidence: 99%

Coding Constraints Modulate Chemically Spontaneous Mutational Replication Gradients in Mitochondrial Genomes

2012

Distances from heavy and light strand replication origins determine duration mitochondrial DNA remains singlestranded during replication. Hydrolytic deaminations from A->G and C->T occur more on single- than doublestranded DNA. Corresponding replicational nucleotide gradients exist across mitochondrial genomes, most at 3rd, least 2nd codon positions. DNA singlestrandedness during RNA transcription causes gradients mainly in long-lived species with relatively slow metabolism (high transcription/replication ratios). Third codon nucleotide contents, evolutionary results of mutation cumulation, follow replicational, not transcriptional gradients in Homo; observed human mutations follow transcriptional gradients. Synonymous third codon position transitions potentially alter adaptive off frame information. No mutational gradients occur at synonymous positions forming off frame stops (these adaptively stop early accidental frameshifted protein synthesis), nor in regions coding for putative overlapping genes according to an overlapping genetic code reassigning stop codons to amino acids. Deviation of 3rd codon nucleotide contents from deamination gradients increases with coding importance of main frame 3rd codon positions in overlapping genes (greatest if these are 2nd position in overlapping genes). Third codon position deamination gradients calculated separately for each codon family are strongest where synonymous transitions are rarely pathogenic; weakest where transitions are frequently pathogenic. Synonymous mutations affect translational accuracy, such as error compensation of misloaded tRNAs by codon-anticodon mismatches (prevents amino acid misinsertion despite tRNA misacylation), a potential cause of pathogenic mutations at synonymous codon positions. Indeed, codon-family-specific gradients are inversely proportional to error compensation associated with gradient-promoted transitions. Deamination gradients reflect spontaneous chemical reactions in singlestranded DNA, but functional coding constraints modulate gradients.

“…These mitogenes are excluded from correlation analyses. To compare syntenies calculated on different sample sizes (meaning different numbers of candidate homologs), Pearson correlation coefficients are z-transformed, and these z values are adjusted for sample sizes to za as explained in Table 3 and previously (Seligmann et al, 2007).…”

Section: Synteny Between Ranked Gene and Alignment Ordersmentioning

confidence: 99%

Syntenies Between Cohosted Mitochondrial, Chloroplast, and Phycodnavirus Genomes: Functional Mimicry and/or Common Ancestry?

2019

DNA and Cell Biology

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Recent analyses suggest bacterial and/or mitochondrion-like ancestry for giant viruses (Megavirales sensu latu): amoeban mitochondrial gene arrangements resemble those of their candidate homologs in megaviral genomes. This presumed ancestral synteny decreases with genome size across megaviral families at large and within Poxviridae. In this study, analyses focus on Phycodnaviridae, a polyphyletic group of giant viruses infecting Haplophyta, Stramenopiles, and other algae, using syntenies between algal mitogene arrangements and chloroplast genomes and Rickettsia prowazekii as positive controls. Mitogene alignment qualities with Rickettsia are much higher than with viral genomes. Mitogenome synteny with some viruses is higher, for others lower than with Rickettsia, despite lower alignments qualities. In some algae, syntenies among cohosted chloroplast, virus, and mitochondrion are higher, in others lower than expected. This suggests gene order coevolution in cohosted genomes, different coregulations of organelle metabolisms for different algae, and viral mitogenome mimicry, to hijack organelle-committed cellular resources and/or escape cellular defenses/genetic immunity systems. This principle might explain high synteny between human mitochondria and the pathogenic endocellular alphaproteobacterium R. prowazekii beyond common ancestry. Results indicate that putative bacteria/mitochondrion-like genomic ancestors of Phycodnaviridae originated before or at the mitochondrionbacteria split, and ulterior functional constraints on gene arrangements of cohosted genomes.