Biology subjects

Knorre, D. A.

Publications and source records attributed to Knorre, D. A..

4 recordsLinked to original sources

bioRxiv2025

Rapid divergence of male and female mitochondrial genomes in a basal protobranch bivalve Yoldia hyperborea

Doubly uniparental inheritance (DUI) of mitochondrial DNA (mtDNA) is a mode of mtDNA transmission whereby the male mitogenome is inherited predominately by males and the female mitogenome is inherited by females. DUI is unique to bivalve mollusks and has been identified in all major bivalve clades, including Protobranchia, the most basal bivalve subclade. Meanwhile, the mechanisms underlying the emergence and evolution of DUI remain poorly understood. Here, we focus on the early stages of divergence of male and female mitochondrial genomes by sequencing them in a basal Protobranchia species Yoldia hyperborea where they are characterized by low level of divergence, suggesting a recent origin of this system. Despite the relatively high relatedness of female and male genomes, we find that they have undergone rapid divergence both on the sequence and the structural level, including an origin of a novel gene, the ORFan, in the male genome. This novel gene is functional, as evidenced by the fact that it is transcribed and is subject to purifying selection. We show that this gene is a result of duplication and rapid evolution of another mitochondrial gene, NAD2. Additionally, the female mitogenome carries a duplicated cassette containing the cytochrome b gene, resulting in two different transcripts in female gonads both of which are subject to purifying selection, although their transcription levels differ by two orders of magnitude. These results showcase the rapid evolution of mitochondrial genes following their duplication, which occurred near the time of divergence of M- and F- mitochondrial genomes within a doubly uniparental inheritance system.

evolutionary biology↗

bioRxiv2024

Inheritance bias of deletion-harbouring mtDNA in yeast: the role of copy number and intracellular selection

Eukaryotic cells contain multiple copies of mitochondrial DNA (mtDNA) molecules that replicate independently. Cell mtDNA content and variability contributes to the overall cell fitness. During sexual reproduction, fungi usually inherit mtDNA from both parents, however, the distribution of the mtDNA in the progeny can be biased toward some mtDNA variants. For example, crossing Saccharomyces cerevisiae strain carrying wild type (rho+) mtDNA with the strain carrying mutant mtDNA variant with large deletion (rho-) can produce up to 99-100% of rho- diploid progeny. Two factors could contribute to this phenomenon. First, rho- cells may accumulate more copies of mtDNA molecules per cell than wild-type cells, making rho- mtDNA a prevalent mtDNA molecule in zygotes. This consequently leads to a high portion of rho - diploid cells in the offspring. Second, rho- mtDNA may have a competitive advantage within heteroplasmic cells, and therefore could displace rho+ mtDNA in a series of generations, regardless of their initial ratio. To assess the contribution of these factors, we investigated the genotypes and phenotypes of twenty two rho- yeast strains. We found that indeed rho- cells have a higher mtDNA copy number per cell than rho+ strains. Using an in silico modelling of mtDNA selection and random drift in heteroplasmic yeast cells, we assessed the intracellular fitness of mutant mtDNA variants. Our model indicates that both higher copy numbers and intracellular fitness advantage of the rho- mtDNA contribute to the biased inheritance of rho- mtDNA.

genetics↗

bioRxiv2023

ORFanes in mitochondrial genomes of marine polychaete Polydora

Most characterised metazoan mitochondrial genomes are compact and encode a small set of proteins that are essential for oxidative phosphorylation. However, in rare cases, invertebrate taxa have additional open reading frames (ORFs) in their mtDNA sequences. Here, we sequenced and analysed the mitochondrial genome of a polychaete worm, Polydora cf. ciliata, part of whose life cycle takes place in low-oxygen conditions. In the mitogenome, we found three "ORFane" regions (1063, 427, and 519 bp) that have no resemblance to any standard metazoan mtDNA gene but lack stop codons in one of the reading frames. Similar regions are found in the mitochondrial genomes of three other Polydora species and Bocardiella hamata. All five species share the same gene order in their mitogenomes, which differ from that of other known spionidae mitogenomes. By analysing the ORFane sequences, we found that they are under negative selection pressure, contain conservative regions, and harbour predicted transmembrane domains.The codon adaptation indices (CAIs) of the ORFan genes were in the same range of values as the CAI of conventional protein-coding genes in corresponding mitochondrial genomes. Together, this suggests that ORFanes encode functional proteins. We speculate that the ORFanes originated from the conventional mitochondrial protein-coding genes which were duplicated when the Polydora/Bocardiella species complex separated from the rest of the Spionidae. Significance statementMetazoan mitochondrial genomes usually contain a conservative set of genes and features. However, mitogenomes of some species contain ORFanes - putative protein-coding genes without clear homology with other known sequences. In this study, we analysed three ORFanes in mitochondria of species of the genera Polydora and Bocardiella, which were absent in all other representatives of Spionidae. To the best of our knowledge, ORFanes havent been described in Annelida before. Sequence analysis of the ORFanes suggests they contain conservative regions and are likely translated into functional proteins. Our study features an uncommon case where new protein-coding genes emerged in the mitochondrial genomes of metazoa.

evolutionary biology↗

bioRxiv2021

The adaptive role of cell death in yeast communities stressed with macrolide antifungals

Microorganisms cooperate with each other to protect themselves from environmental stressors. An extreme case of such cooperation is regulated cell death for the benefit of other cells. Dying cells can provide surviving cells with nutrients or induce their stress-response by transmitting an alarm signal; however, the role of dead cells in microbial communities is unclear. Here we searched for types of stressors the protection from which can be achieved by death of a subpopulation of cells. Thus, we compared the survival of Saccharomyces cerevisiae cells upon exposure to various stressors in the presence of additionally supplemented living versus dead cells. We found that dead cells contribute to yeast community resistance against macrolide antifungals (e.g. amphotericin B [AmB] and filipin) to a greater extent than living cells. Dead yeast cells absorbed more macrolide filipin than control cells because they exposed intracellular sterol-rich membranes. We also showed that, upon the addition of lethal concentrations of AmB, supplementation with AmB-sensitive cells but not with AmB-resistant cells enabled the survival of wild-type cells. Together, our data suggests that cell-to-cell heterogeneity in sensitivity to AmB can be an adaptive mechanism helping yeast communities to resist macrolides, which are naturally occurring antifungal agents. ImportanceEukaryotic microorganisms harbour elements of programmed cell death (PCD) mechanisms that are homologous to the PCD of multicellular metazoa. However, it is still debated whether microbial PCD has an adaptive role or the processes of cell death are an aimless operation in self-regulating molecular mechanisms. Here, we demonstrated that dying yeast cells provide an instant benefit for their community by absorbing macrolides, which are bacteria-derived antifungals. Our results illustrate the principle that the death of a microorganism can contribute to the survival of its kin and suggest that early plasma membrane permeabilization improves community-level protection. The latter makes a striking contrast to the manifestations of apoptosis in higher eukaryotes, the process by which plasma membranes maintain integrity.

microbiology↗