Mitochondrial DNA Research Articles

Melita panda, a new species of Melitidae (Crustacea, Amphipoda) from Japan

A new intertidal species of the melitid amphipod, Melita panda, from the Wakayama Prefecture, Japan, is identified and described. Melita pandasp. nov. differs from the similar M. koreana and M. nagatai by its black-and-white body color, well-developed anterodistal projection of the male gnathopod 1 propodus, and telson armature. Molecular phylogenetic analyses based on the nuclear 28S rRNA and mitochondrial COI genes support that M. pandasp. nov. is closely related to M. koreana and M. nagatai.

The complete mitochondrial genome of Uroobovella oviformis (Kontschan & Stary, 2011) (Acari, Urodinychidae) and its phylogenetic position within the order Mesostigmata

ABSTRACT Mitochondrial genomes are highly conserved in genetic processes and serve as a useful molecular marker for phylogenetic and evolutionary analysis. In this study, the complete mitochondrial genome of Uroobovella oviformis was sequenced and annotated. The mitochondrial genome is a closed, double-stranded circular molecule of 14,306 bp length and contains the typical 37 genes. All of the protein-coding genes started with ATN and terminated with TAA except COX2, COX3, and CYTB, which stopped with single T. The whole mitochondrial genome of U. oviformis showed a heavy AT nucleotide bias (77.69%), a positive AT-Skew (0.035), and a negative GC-Skew (−0.320), as well as translocation of seven genes including CYTB and ND6. The phylogenetic tree was constructed by Bayesian inference and maximum likelihood methods using three different datasets (PCG, PCG12, and AA), which were constructed to discuss the phylogenetic status of Mesostigmata. The analysis showed that the branching relationships among the six trees were consistent and all families except the Laelapidae were recovered as monophyletic. Furthermore, U. oviformis forms a separate clade and is located at the base of Mesostigmata and has a closer relationship with Antennophorina.

Oxazolidinone antibiotics impair ex vivo megakaryocyte differentiation from hematopoietic progenitor cells and their maturation into platelets

ABSTRACT Oxazolidinones (linezolid and tedizolid) adverse reactions include thrombocytopenia, the mechanism of which is still largely unknown. In cultured cells, oxazolidinones impair mitochondrial protein synthesis and oxidative metabolism. As mitochondrial activity is essential for megakaryocyte differentiation and maturation into platelets, we examined whether oxazolidinones impair these processes ex vivo and alter, in parallel, the activity of mitochondrial cytochrome c -oxidase (CYTOX; enzyme partly encoded by the mitochondrial genome) and cell morphology. Human CD34+ cells were isolated, incubated with cytokines (up to 14 days) and clinically relevant oxazolidinone concentrations or in control conditions, and used for (i) clonogenic assays [counting of megakaryocyte (CFU-Mk), granulocyte-monocyte (CFU-GM), burst-forming unit-erythroid (BFU-E) colonies]; (ii) the measure of the expression of megakaryocyte surface antigens (CD34 to CD41 and CD42); (iii) counting of proplatelets; (iv) the measurement of CYTOX activity; and (v) cell morphology (optic and electron microscopy). Oxazolidinones caused a significant decrease in BFU-E but not CFU-Mk or CFU-GM colonies. Yet, the megakaryocytic lineage was markedly affected, with a decreased differentiation of CD34+ into CD41+/CD42+ cells, an abolition of proplatelet formation and striking decrease in the numbers of large polylobulated nucleus megakaryocytes, with a complete loss of intracellular demarcation membrane system, disappearance of mitochondria, and suppression of CYTOX activity. These alterations were more marked in cells incubated with tedizolid than linezolid. These data suggest that oxazolidinones may induce thrombocytopenia by impairing megakaryocytic differentiation through mitochondrial dysfunction. Pharmacological interventions to prevent this toxicity might therefore be difficult as mitochondrial toxicity is most probably inherently linked to their antibacterial activity.

Cytoplasmic male sterility in plants with special emphasis on sugar beet

The phenomenon of cytoplasmic male sterility (CMS) in plants is characterized by a disturbance in the development of functional pollen. The cause of this disorder is the incompatibility of the mitochondrial and nuclear genome. Determinants of CMS are found in the mitochondrial genome and are inherited maternally. Nuclear Rf genes are responsible for restoring male fertility in CMS plants most often by posttranscriptional and/or posttranslational activity on mitochondrial gene expression. Two fertility restoring genes have been identified in sugar beet plants, of which Rf1 is the best characterized. It is concluded that the translation product of this gene acts as a molecular chaperone leading to inactivation of a specific mitochondrial protein that is a marker for the CMS trait in sugar beet. The CMS phenomenon is applied in the commercial breeding of hybrid varieties of many crop species. Exploiting heterosis is easier with the knowledge of cytoplasmic (mitochondrial) determinants of sterility and corresponding restorer genes.

The genome sequence of the ruby bryozoan, Bugula neritina (Linnaeus, 1758)

We present a genome assembly from a specimen of Bugula neritina (the ruby bryozoan; Bryozoa; Gymnolaemata; Cheilostomatida; Bugulidae). The genome sequence has total length of 216.00 megabases. Most of the assembly is scaffolded into 9 chromosomal pseudomolecules. The mitochondrial genome has also been assembled and is 15.25 kilobases in length. Gene annotation of this assembly on Ensembl identified 20,264 protein-coding genes.

The genome sequence of the European conger eel, Conger conger (Linnaeus, 1758)

We present a genome assembly from an individual Conger conger (the European conger eel; Chordata; Actinopteri; Anguilliformes; Congridae). The genome sequence spans 1,136.40 megabases. Most of the assembly is scaffolded into 19 chromosomal pseudomolecules. The mitochondrial genome has also been assembled and is 18.86 kilobases in length.

The genome sequence of the Pale Oak Beauty, Hypomecis punctinalis (Scopoli, 1763)

We present a genome assembly from an individual male Hypomecis punctinalis (the Pale Oak Beauty; Arthropoda; Insecta; Lepidoptera; Geometridae). The genome sequence has a total length of 741.20 megabases. Most of the assembly is scaffolded into 30 chromosomal pseudomolecules, including the Z sex chromosome. The mitochondrial genome has also been assembled and is 15.64 kilobases in length. Gene annotation of this assembly on Ensembl identified 13,897 protein-coding genes.

The genome sequence of the Bindweed Bent-wing moth, Bedellia somnulentella (Zeller, 1847)

We present a genome assembly from an individual female Bindweed Bent-wing moth, Bedellia somnulentella (Arthropoda; Insecta; Lepidoptera; Bedelliidae). The genome sequence has a length of 549.00 megabases. Most of the assembly is scaffolded into 31 chromosomal pseudomolecules, including the W and Z sex chromosomes. The mitochondrial genome has also been assembled and is 16.62 kilobases in length. Gene annotation of this assembly on Ensembl identified 11,959 protein-coding genes.

The genome sequence of an Entiminae weevil, Polydrusus pterygomalis Boheman, 1840

We present a genome assembly from an individual female Entiminae weevil, Polydrusus pterygomalis (Arthropoda; Insecta; Coleoptera; Curculionidae). The genome sequence has a total length of 1,051.50 megabases. Most of the assembly is scaffolded into 11 chromosomal pseudomolecules, including the X sex chromosome. The mitochondrial genome has also been assembled and is 20.95 kilobases in length.

Whole genome sequence analysis of population structure and insecticide resistance markers in Anopheles melas from the Bijagós Archipelago, Guinea-Bissau

BackgroundAnopheles melas is an understudied malaria vector with a potential role in malaria transmission on the Bijagós Archipelago of Guinea-Bissau. This study presents the first whole-genome sequencing and population genetic analysis for this species from the Bijagós. To our knowledge, this also represents the largest population genetic analysis using WGS data from non-pooled An. melas mosquitoes.MethodsWGS was conducted for 30 individual An. melas collected during the peak malaria transmission season in 2019 from six different islands on the Bijagós Archipelago. Bioinformatics tools were used to investigate the population structure and prevalence of insecticide resistance markers in this mosquito population.ResultsInsecticide resistance mutations associated with pyrethroid resistance in Anopheles gambiae s.s. from the Bijagós were absent in the An. melas population, and no signatures of selective sweeps were identified in insecticide resistance-associated genes. Analysis of structural variants identified a large duplication encompassing the cytochrome-P450 gene cyp9k1. Phylogenetic analysis using publicly available mitochondrial genomes indicated that An. melas from the Bijagós split into two phylogenetic groups because of differentiation on the mitochondrial genome attributed to the cytochrome C oxidase subunits COX I and COX II and the NADH dehydrogenase subunits 1, 4, 4L and 5.ConclusionsThis study identified an absence of insecticide-resistant SNPs common to An. gambiae in the An. melas population, but did identify structural variation over insecticide resistance-associated genes. Furthermore, this study presents novel insights into the population structure of this malaria vector using WGS analysis. Additional studies are required to further understand the role of this vector in malaria transmission.Graphical abstract

The genome sequence of yellow bugle, Ajuga chamaepitys (L.) Schreb. (Lamiaceae)

We present a genome assembly from an individual Ajuga chamaepitys (yellow bugle; Streptophyta; Magnoliopsida; Lamiales; Lamiaceae). The genome sequence has a total length of 891.60 megabases. Most of the assembly is scaffolded into 14 chromosomal pseudomolecules. The mitochondrial and plastid genome assemblies have lengths of 418.31 kilobases and 150.7 kilobases, respectively. Gene annotation of this assembly on Ensembl identified 23,755 protein-coding genes.

The genome sequence of barren brome, Bromus sterilis L. (Poaceae)

We present a genome assembly from an individual Bromus sterilis (the barren brome; Streptophyta; Magnoliopsida; Poales; Poaceae). The genome sequence has a total length of 2,677.90 megabases. Most of the assembly is scaffolded into 7 chromosomal pseudomolecules. The mitochondrial and plastid genome assemblies have lengths of 523.28 kilobases and 136.96 kilobases, respectively. Gene annotation of this assembly on Ensembl identified 29,147 protein-coding genes.

The first report of complete mitogenomes of two endangered species of genus Propomacrus (Coleoptera: Scarabaeidae: Euchirinae) and phylogenetic implications.

To understand the mitochondrial genome structure of two endangered and long-armed scarab beetles, Propomacrus davidi and Propomacrus bimucronatus, their complete mitogenomes were sequenced for the first time in this study. The complete mitogenomes of P. davidi and P. bimucronatus were 18, 042 bp and 18, 104 bp in length, respectively. The gene orders of their mitogenomes were highly consistent with other Coleopteran species, and the typical ATN was used as the start codon in most protein coding genes. The incomplete stop codon T was used in cox1, cox2, and nad5, and TAN was used as a complete stop codon in most protein coding genes. All predicted tRNAs could form a typical cloverleaf secondary structure, except that trnS1 lacked the dihydrouridine arm. Based on the maximum likelihood and the Bayesian inference methods, phylogenetic trees of 50 species were reconstructed. The results showed that P. davidi, P. bimucronatus, Cheirotonus jansoni and Cheirotonus gestroi clustered in the same branch, and were the most closely related. The results supported that subfamily Euchirinae is a monophyletic group of Scarabaeidae, which was consistent with the morphological classification. These molecular data enriched the complete mitogenome database of Euchirinae, and improved our understanding of the phylogenetic relationship and evolutionary characteristics of these two endangered species.

The Role and Research Progress of Mitochondria in Sensorineural Hearing Loss.

Hearing loss is one of the most common human diseases, seriously affecting everyday lives. Mitochondria, as the energy metabolism center in cells, are also involved in regulating active oxygen metabolism and mediating the occurrence of inflammation and apoptosis. Mitochondrial defects are closely related to hearing diseases. Studies have shown that mitochondrial DNA mutations are one of the causes of hereditary hearing loss. In addition, changes in mitochondrial homeostasis are directly related to noise-induced hearing loss and presbycusis. This review mainly summarizes and discusses the effects of mitochondrial dysfunction and mitophagy on hearing loss. Subsequently, we introduce the recent research progress of targeted mitochondria therapy in the hearing system.

Genetic Diversity, Kinship, and Polychromatism in the Spotted Eagle Ray Aetobatus ocellatus of Fiji

The spotted eagle ray Aetobatus ocellatus (Kuhl, 1923) has a widespread Indo-West Pacific distribution and displays substantial population genetic structuring. Genetic data are crucial for understanding the species’ diversity, connectivity, and adaptation. However, molecular genetic information on A. ocellatus from Melanesia is lacking, which impedes our understanding of gene flow among geographic regions. In this study, we sampled 45 A. ocellatus, primarily from Fiji’s largest fish market in the capital, Suva. Mitochondrial DNA Cytochrome C Oxidase subunit I (COI) barcoding was used for species identification, and DArT-seqTM technology was applied to assess the nuclear genetic diversity. Barcoding of the COI gene showed a 98.6% to 99.8% similarity to A. ocellatus reference sequences in the Barcode of Life Data System, and the 45 individuals were represented by three major evolutionary haplotype clusters. Genotyping resulted in 24,313 Single-Nucleotide Polymorphisms (SNPs) which were quality-filtered to 7094 SNPs per individual. The observed heterozygosity level was 0.310. The inbreeding coefficient was positive, and genotyping identified one full-sibling pair and one half-sibling pair from the 45 individuals. Additionally, eagle rays exhibit polychromatic patterns, and at least three ventral pattern variations were recorded in specimens from the market. Collectively, our main findings characterize the genetic profile of A. ocellatus in Fiji and can help to understand the diversification of this species within the region.

“Internal Trouble and Outside Aggression” Strategy: Energy Deprivation Synergized With cGAS‐STING Pathway Activation for Stimuli‐Responsive Photodynamic‐Metal‐Metabolic Immunotherapy

AbstractThe aberrant metabolic activities of tumor cells not only facilitate tumor proliferation but also impair immune cell function and cause an immunosuppressive tumor microenvironment (TME). Thus, reshaping the metabolic TME while activating innate immunity is highly desirable but challenging. Herein, a multifunctional immunomodulator is engineered for near‐infrared light (NIR)‐triggered photodynamic‐metal‐metabolic immunotherapy via the “internal trouble and outside aggression” strategy. Specifically, an endogenous and exogenous stimuli‐responsive nanoagent is prepared consisting of photosensitizer chlorin e6 (Ce6) modified dense silica‐coated rare earth‐doped nanoparticles (ReNPs@SiO2(Ce6)), with in situ grown ZIF‐8 on the surface for loading glucose transporter‐1 (GLUT‐1) inhibitor Fasentin and glutaminase‐1 inhibitor bis‐2‐(5‐phenylacetamido‐1,3,4‐thiadiazol‐2‐yl)ethyl sulfide (BPTES). The as‐obtained final product is denoted as ReSZ(FB). ReSZ(FB) induces‐ mitochondrial damage and releases mitochondrial DNA (mtDNA) via NIR‐mediated PDT. Subsequently, Zn2+ from ZIF‐8 collaborates with mtDNA to activate the cGAS‐STING pathway, initiating a robust tumor‐specific immune response. Concurrently, Fasentin and BPTES triggeres energy deprivation by blocking glucose uptake and inhibiting glutamine decomposition, thereby reprogramming the metabolic TME, and alleviating immunosuppression. Tumor cells are damaged and trapped into “internal trouble” by combining PDT and energy deprivation, while the sharply enhanced immune cell lethality exposes cancer cells to “outside aggression”. Overall, this photodynamic‐metal‐metabolic immunotherapy provides a promising paradigm for cancer therapy.

Biomarkers of mitochondrial stress and DNA damage during pediatric catheter-directed neuroangiography - a prospective single-center study.

Neuroangiography represents a critical diagnostic and therapeutic imaging modality whose associated radiation may be of concern in children. The availability of in vivo radiation damage markers would represent a key advancement for understanding radiation effects and aid in the development of radioprotective strategies. Determine if biomarkers of cellular damage can be detected in the peripheral blood mononuclear cells (PBMC) of children undergoing neuroangiography. Prospective single-site study of 27 children. Blood collected pre and post neuroangiography, from which PBMC were isolated and assayed for biomarkers of mitochondrial stress (mitochondrial membrane potential (MMP), reactive oxygen species (ROS), and mitochondrial DNA (mtDNA)) and DNA damage (γH2AX). Dose response of biomarkers vs. radiation dose was analyzed using linear regressions. The cohort was divided into higher (HD) and lower dose (LD) groups and analyzed using linear mixed models and compared using Welch's t-tests. No biomarker exhibited a dose-dependent response following radiation (γH2AX: R2 = 0.0012, P = 0.86; MMP: R2 = 0.016, P = 0.53; mtDNA: R2 = 0.10, P = 0.11; ROS: R2 = 0.0023, P = 0.81). Groupwise comparisons showed no significant differences in γH2AX or ROS after radiation (γH2AX: LD: 0.6 ± 6.0, P = 0.92; HD: -7.5 ± 6.3 AU, P = 0.24; ROS: LD: 1.3 ± 2.8, P = 0.64; HD: -3.6 ± 3.0 AU, P = 0.24). Significant changes were observed to mitochondrial markers MMP (-53.7 ± 14.7 AU, P = 0.0014) and mtDNA (-1.1 ± 0.4 AU, P = 0.0092) for HD, but not the LD group (MMP: 26.1 ± 14.7 AU, P = 0.090; mtDNA: 0.2 ± 0.4, P = 0.65). Biomarkers of mitochondrial stress in PBMC were identified during pediatric neuroangiography and warrant further investigation for radiation biodosimetry. However, isolating radiation-specific effects from those of procedural stress and general anesthesia requires further investigation.

Mitochondrial markers revealed genetic panmixia in the data-deficient yellowfin snapper, Lutjanus xanthopinnis (Actinopterygii: Eupercaria: Lutjanidae), from a hotspot of the southern region of the South China Sea

Understanding the genetic structure and diversity of marine fish is crucial for a sustainable management program. We examined the genetic diversity and historical demographics of the yellowfin snapper, Lutjanus xanthopinnis Iwatsuki, Tanaka et Allen, 2015, in the coastal waters of east Peninsular Malaysia which is bordered by the southern part of the South China Sea using the mitochondrial genes (mtDNA) D-loop and Cytochrome b (Cyt-b). A total of 99 (D-loop) and 78 (Cyt-b) specimens of L. xanthopinnis were successfully sequenced from six locations within the range of species distribution along the Malaysian South China Sea. In the presently reported study, the lack of genetic differentiation among populations can be attributed to historical demographic events, eggs and planktonic larvae’ ability to disperse, spawning patterns, and the absence of physical barriers in the geographical landscape. Maximum likelihood gene trees demonstrated that the populations under study had limited structuring and formed a panmictic population that lacks support for internal clades. The AMOVA (Analysis of Molecular Variance) and population pairwise ФST values indicated high genetic exchange between the study areas. A high level of haplotype diversity (D-loop: 0.948–1.000; Cyt-b: 0.542–0.928), low nucleotide diversity (D-loop: 0.0095–0.0159; Cyt-b: 0.0022–0.0049) and starlike haplotype network indicates a recent expansion of L. xanthopinnis populations in Malaysian South China Sea. However, neutrality and goodness of fit tests revealed non-significant values. Furthermore, the BSP (Bayesian skyline plot) analysis estimated population expansion events during the late Pleistocene. During this epoch, the fluctuation in sea level may have led to an increase in the abundance of resources and favorable habitats for the yellowfin snapper. The presently reported findings could initiate efficient management strategies for L. xanthopinnis along the coastal areas of the Malaysian South China Sea and other nearby nations that share the same waterways.

Maternal Ketone Supplementation Throughout Gestation Improves Neonatal Cardiac Dysfunction Caused by Perinatal Iron Deficiency.

Iron deficiency (ID) is common during gestation and in early infancy and has been shown to adversely affect cardiac development and function, which could lead to lasting cardiovascular consequences. Ketone supplementation has been shown to confer cardioprotective effects in numerous disease models. Here we tested the hypothesis that maternal ketone supplementation during gestation would mitigate cardiac dysfunction in ID neonates. Female Sprague Dawley rats were fed an iron-restricted or iron-replete diet before and throughout pregnancy. Throughout gestation, iron-restricted dams were given either a daily subcutaneous injection of ketone solution (containing β-hydroxybutyrate [βOHB]) or saline (vehicle). Neonatal offspring cardiac function was assessed by echocardiography at postnatal days (PD)3 and 13. Hearts and livers were collected post-mortem for assessments of mitochondrial function and gene expression profiles of markers oxidative stress and inflammation. Maternal iron restriction caused neonatal anemia and asymmetric growth restriction at all time points assessed, and maternal βOHB treatment had no effect on these outcomes. Echocardiography revealed reduced ejection fraction despite enlarged hearts (relative to body weight) in ID offspring, resulting in impaired oxygen delivery, which was attenuated by maternal βOHB supplementation. Further, maternal ketone supplementation affected biochemical markers of mitochondrial function, oxidative stress and inflammation in hearts of neonates, implicating these pathways in the protective effects conferred by βOHB. In summary, βOHB supplementation confers protection against cardiac dysfunction in ID neonates, and could have implications for the treatment of anemic babies.

Atomic vacancies of molybdenum disulfide nanoparticles stimulate mitochondrial biogenesis

Diminished mitochondrial function underlies many rare inborn errors of energy metabolism and contributes to more common age-associated metabolic and neurodegenerative disorders. Thus, boosting mitochondrial biogenesis has been proposed as a potential therapeutic approach for these diseases; however, currently we have a limited arsenal of compounds that can stimulate mitochondrial function. In this study, we designed molybdenum disulfide (MoS2) nanoflowers with predefined atomic vacancies that are fabricated by self-assembly of individual two-dimensional MoS2 nanosheets. Treatment of mammalian cells with MoS2 nanoflowers increased mitochondrial biogenesis by induction of PGC-1α and TFAM, which resulted in increased mitochondrial DNA copy number, enhanced expression of nuclear and mitochondrial-DNA encoded genes, and increased levels of mitochondrial respiratory chain proteins. Consistent with increased mitochondrial biogenesis, treatment with MoS2 nanoflowers enhanced mitochondrial respiratory capacity and adenosine triphosphate production in multiple mammalian cell types. Taken together, this study reveals that predefined atomic vacancies in MoS2 nanoflowers stimulate mitochondrial function by upregulating the expression of genes required for mitochondrial biogenesis.