Mitochondrial DNA Research Articles

Monophyly or Homoplasy? The Relationships of a Rare New Species of Cambeva (Siluriformes: Trichomycteridae) from the Brazilian Atlantic Forest with a Bicolored Caudal Pattern

The Brazilian Atlantic Forest, one the five main biodiversity hotspots in the world, still houses many organisms that are rare and unknown to science, mostly concentrated in mountain ranges. Herein, we describe a rare new species of Cambeva from the Rio Tietê drainage at the Serra da Mantiqueira, exhibiting a caudal fin color pattern comprising a light-yellowish–white bar posteriorly edged by a black pigmented area. A similar color pattern was described for C. castroi, C. diabola, and C. melanoptera, also endemic to the Rio Paraná basin, and considered evidence of close relationships among these three species. However, other morphological characteristics highly suggest that the new species is not closely related to C. castroi, C. diabola, and C. melanoptera). Herein, we perform a molecular phylogenetic analysis using two mitochondrial genes and one nuclear gene, including all species with that bicolored caudal pattern. The analysis strongly supports the new species as a member of the alpha-clade, and therefore as distantly related to those three species belonging to the beta-clade, indicating that this color pattern has homoplastically arisen in Cambeva. The data reported here reinforce the urgent need for field studies to better understand the different evolutionary patterns found in the genus, since an intense process of environmental degradation is in course.

#3001 MtDNA copy number correlates to coronary artery calcium score and biological age in kidney failure patients

Abstract Background and Aims Chronic kidney disease (CKD) and kidney failure are connected to increased oxidative stress and vascular calcification, which are indicators for development of comorbidities and mortality outcome. Mitochondrial (mt)DNA copy number has been reported as independent predictor for frailty and mortality outcome of various cardiovascular diseases (CVD) and cancer. We aimed that mtDNA copy number in whole blood of kidney failure patients can be correlated to coronary artery media calcification score and coronary artery calcium (CAC) score and be used as an independent predictor for comorbidities and mortality outcome. Method Quantitative PCR (qPCR) with TaqMan® probes for three mtDNA genes (mtND1, mtND4 and mtCOX1) and two single locus genes on nuclear DNA (hemoglobin subunit beta and 18S), for normalization, is performed on DNA samples isolated from collected blood of 196 kidney transplant donors and 211 recipients at basal timepoint and 32 at 1-year-follow-up timepoint, included in the KaroKidney biobank. Resulting mtDNA copy number is investigated for correlation to CAC score, patient mortality outcome, biological age determined by skin autofluorescence and other clinical parameters. Results In our Swedish kidney transplant cohort we can see statistically significant difference in mtDNA copy number between kidney failure patients (recipients) and healthy controls (donors). No obvious difference between females and males was observed. mtDNA copy number correlates to biological age determined by skin autofluorescence, CAC score and Framingham CVD risk score. In the 32 1-year-follow-up samples we could see significant increase/recovery of mtDNA copy number for male patients compared to their baseline before receiving a transplant. Conclusion In this study we show that mtDNA copy number in kidney failure patients correlates to biological age and CAC score, affirming mtDNA copy number as an independent predictor of frailty in this Swedish cohort of CKD patients. Additionally, we can see that a kidney transplant can lead to a significant increase of mtDNA copy number in blood one year later, suggesting a general increase in health quality.

The Identification of the Mitochondrial DNA Polymerase γ (Mip1) of the Entomopathogenic Fungus Metarhizium brunneum

Replication of the mitochondrial (mt) genome in filamentous fungi is under-studied, and knowledge is based mainly on data from yeasts and higher eukaryotes. In this study, the mitochondrial DNA polymerase γ (Mip1) of the entomopathogenic fungus Metarhizium brunneum is characterized and analyzed with disruption experiments and its in silico interactions with key proteins implicated in mt gene transcription, i.e., mt RNA polymerase Rpo41 and mt transcription factor Mtf1. Disruption of mip1 gene and its partial expression influences cell growth, morphology, germination and stress tolerance. A putative in silico model of Mip1-Rpo41-Mtf1, which is known to be needed for the initiation of replication, was proposed and helped to identify potential amino acid residues of Mip1 that interact with the Rpo41-Mtf1 complex. Moreover, the reduced expression of mip1 indicates that Mip1 is not required for efficient transcription but only for replication. Functional differences between the M. brunneum Mip1 and its counterparts from Saccharomyces cerevisiae and higher eukaryotes are discussed.

Historical imprints on genetic population structure in direct-developing beach whelks (Bullia digitalis)

Marine organisms often show deep genetic divergence between lineages that are characterized by shallow population structure. The distinction of historical and contemporary demographic forces in creating and maintaining these genetic patterns is crucial for management and conservation. In this study, we examined the genetic population structure of Bullia digitalis, a lecithotrophic sandy beach whelk that lacks a pelagic larval phase and is thus expected to show limited connectivity between populations. Mitochondrial (mt)DNA cytochrome c oxidase subunit I (COI; 540 bp, n = 214) and a reanalysis of allozyme data (14 loci, n = 735) among populations along the cool southeast Atlantic (west) and warm-temperate southwest Indian Ocean (south) coasts of southern Africa showed a strong phylogeographic break across Cape Point with mtDNA (ΦRT = 0.6, p < 0.001), but a weak break with allozymes (FRT = 0.002, p = 0.004). MtDNA gene flow occurred asymmetrically from the west to the south coast. Although there was no mtDNA differentiation between populations on either side of that break (ΦSR = 0.0), there was weak but significant isolation by distance (IBD) among south coast samples (r2 = 0.20, p = 0.039). In contrast, significant allozyme differentiation was detected on small spatial scales but without overall IBD. MtDNA mismatch analysis indicated a recent range expansion, suggesting historic population expansions, most likely during periods of lower sea levels and greater habitat continuity along southern African shores. Thus, the apparent mtDNA connectivity among populations of beach whelks likely reflects historic, rather than contemporary, gene flow.

Riverscape features determining the genetic structure of the Yellow‐Spotted Amazon River Turtle (Podocnemis unifilis) in Brazilian Amazonia

AbstractLandscape characteristics can influence gene flow depending on the species ability to disperse. This imposes different levels of resistance to movement, determining the genetic structure and diversity of populations. Waterfalls and rapids in the Amazon basin have been suggested as contributing factors to the diversification and genetic structure of freshwater species, including turtles. Thus, along some main rivers of the Brazilian Amazon: Juruá, Madeira, Amazonas, Trombetas, Tapajós, Xingu, Tocantins, and Araguaia, we evaluated the spatial distribution of genetic diversity and characterized the population structure of Podocnemis unifilis, a widely distributed and endangered Amazonian turtle, using the mitochondrial DNA control region. We tested for isolation by geographic distance and by resistance models through an integrative approach using genetic, geographic, and ecological data, comparing these matrices with genetic distance. We found heterogeneous levels of genetic diversity and no spatial patterns. Results supported the isolation by resistance hypothesis, where the movement of individuals was influenced by freshwater, vegetational, climatological, and geomorphological variables, explaining the genetic distance of P. unifilis. Rapids and waterfalls impose greater resistance although they are barriers with different levels of permeability to the P. unifilis gene flow. Thus, the idiosyncrasies of each sub‐basin must be considered in the interpretation of the patterns found in assessing phylogeographic history.Abstract in Portuguese is available with online material.

Optimizing resuscitation of the donation after circulatory death heart by mitochondrial protection in a female porcine model.

Due to the shortage of donor organs, an increasing number of transplant organs are harvested after circulatory arrest (donation after circulatory death, DCD). Using a translational porcine DCD model, we developed and evaluated a protocol based on cardioprotection by multi-drug postconditioning to optimize resuscitation of DCD hearts by ex situ heart perfusion (ESHP). Hearts of female pigs (45.0±4.5 kg) were procured following a clinically identical DCD protocol, consisting of the termination of ventilator support and confirmation of circulatory arrest, followed by a 15-min standoff period. DCD hearts were randomly allocated to ESHP (38.4°C) in the absence (untreated, N=5) or presence (treated, N=5) of a postconditioning treatment added to the perfusate, consisting of Intralipid (1%), sevoflurane (2% v/v), and remifentanil (3 nM). All hearts were perfused with blood and Krebs-Henseleit solution (1:1) for 60 min in Langendorff mode and for additional 300 min in working mode for a total perfusion time of 6 hrs. Oxidative capacity and detailed left ventricular (LV) mechanical function under increasing workload (left atrial pressure 6-12 mmHg) were assessed hourly. LV tissue was snap-frozen at the end of ESHP and used for molecular analyses. LV inotropy (LVdP/dtmax) did not decline over time in treated DCD hearts and was significantly higher at the end of the protocol as compared with untreated DCD hearts (ΔLVdP/dtmax= 440 mmHg/s, p=0.009). Treated DCD hearts exhibited persistently higher LV stroke work index (LVSWI) during the 6-hr period of ESHP, whereas untreated DCD hearts displayed a significant decline (ΔLVSWI=-3.10 mL*mmHg/g, p(time within untreated group)<0.001). Treated DCD hearts displayed higher metabolic activity as measured by oxygen consumption (ΔO2=3.11 mL O2/min/100g; p=0.004), and released lower amounts of cell-free mitochondrial DNA into the perfusate, a marker of potential graft dysfunction. Treated hearts also used fatty acids from Intralipid as an energy source, while untreated DCD hearts showed glyceroneogenesis with triglyceride accumulation and depletion of tricarboxylic acid cycle intermediates, reduced mitochondrial complex I, II, and III activities with accumulation of mitochondrial NADH, and signs of ultrastructural damage. A translationally relevant protective ESHP protocol consisting of treatment with Intralipid, sevoflurane, and remifentanil markedly accelerated functional recovery and improved viability of DCD hearts.

Molecular and morphological examinations show diversity in the genus Amphidromus (Camaenidae: Stylommatophora) in Bangladesh

Establishing a robust taxonomic foundation is crucial for biodiversity conservation. Bangladesh harbours potentially unique biodiversity that remains inadequately explored. Concurrently, its biodiversity faces substantial pressure owing to environmental changes; thus, an urgent assessment of its current status is required. In this study, we focused on the understudied land snails of Bangladesh, the genus Amphidromus. Utilizing 45 samples collected from 13 sites during a 2018–2022 survey, as well as museum specimens and literature sources, we conducted molecular phylogenetic analyses and the haplotype network of the mitochondrial 16S ribosomal RNA, cytochrome c oxidase subunit I and nuclear internal transcribed spacer 1, examined shell shapes using elliptical Fourier features, and evaluated shell size and band patterns. Based on the molecular and morphological examinations, we identified five Amphidromus species in Bangladesh, including two potentially undescribed species, each recorded at a single site in the Chittagong Division. The dominant species, A. globonevilli, is widely distributed in central and eastern Bangladesh, revealing a geographically structured mitochondrial DNA diversity. Furthermore, in the museum specimens, we confirmed the occurrence of A. sinensis vicaria and A. sylheticus, the latter being newly discovered in Bangladesh. These two species may be limited to the eastern part of Bangladesh and represent low-density species. Although the taxonomic relationship of these species with A. globonevilli remains unclear and further studies with molecular data are warranted, our findings provide the basis for further understanding and conservation of biodiversity in Bangladesh.

#1868 Dapagliflozin reduces urinary kidney injury biomarkers in chronic kidney disease irrespective of albuminuria level

Abstract Background and Aims The beneficial effects of Sodium-Glucose Cotransporter 2(SGLT2) inhibitor in patients with chronic kidney disease (CKD) with low albuminuria levels have not been established. In this study, we aimed to compare the effects of dapagliflozin on kidney injury biomarkers in patients with CKD stratified by albuminuria level. Method We prospectively enrolled healthy volunteers (HVs) (n = 20) and patients with CKD (n = 54) with and without diabetes mellitus (DM). Patients with CKD were divided into two subgroups by age- and sex-matched according to urinary albumin-creatinine ratio (uACR) levels (&amp;lt;300 mg/g and ≥300 mg/g). The CKD group received dapagliflozin 10 mg per day. Urine samples were collected before treatment and after 3 months and 6 months of dapagliflozin. Urinary kidney injury molecule-1 (KIM-1), interleukin-1β (IL-1β), and mitochondrial DNA nicotinamide adenine dinucleotide dehydrogenase subunit-1 (mtND1) copy number were measured. Results The estimated glomerular filtration rate (eGFR) of patients with CKD was lower than that of HVs (p &amp;lt; 0.001). During the study period, eGFR decreased and uACR did not change in the CKD group. Kidney injury markers were significantly elevated in patients with CKD compared with those in HVs. Dapagliflozin reduced urinary KIM-1, IL-1β and mtDNA copy number in patients with CKD after 6 months of treatment. In further, the levels of urinary KIM-1 and IL-1β, patients with CKD decreased after 6 months of dapagliflozin treatment regardless of albuminuria level. Conclusion In this study, dapagliflozin reduced urinary kidney injury biomarkers in patients with CKD, regardless of albuminuria level. These findings suggest that SGLT2i may also attenuate the progression of low albuminuric CKD.

Origins of tissue and cell-type specificity in mitochondrial DNA (mtDNA) disease.

Mutations of mitochondrial (mt)DNA are a major cause of morbidity and mortality in humans, accounting for approximately two thirds of diagnosed mitochondrial disease. However, despite significant advances in technology since the discovery of the first disease-causing mtDNA mutations in 1988, the comprehensive diagnosis and treatment of mtDNA disease remains challenging. This is partly due to the highly variable clinical presentation linked to tissue-specific vulnerability that determines which organs are affected. Organ involvement can vary between different mtDNA mutations, and also between patients carrying the same disease-causing variant. The clinical features frequently overlap with other non-mitochondrial diseases, both rare and common, adding to the diagnostic challenge. Building on previous findings, recent technological advances have cast further light on the mechanisms which underpin the organ vulnerability in mtDNA diseases, but our understanding is far from complete. In this review we explore the origins, current knowledge, and future directions of research in this area.

Illuminating mitochondrial translation through mouse models.

Mitochondria are hubs of metabolic activity with a major role in ATP conversion by oxidative phosphorylation (OXPHOS). The mammalian mitochondrial genome encodes 11 mRNAs encoding 13 OXPHOS proteins along with 2 rRNAs and 22 tRNAs, that facilitate their translation on mitoribosomes. Maintaining the internal production of core OXPHOS subunits requires modulation of the mitochondrial capacity to match the cellular requirements and correct insertion of particularly hydrophobic proteins into the inner mitochondrial membrane. The mitochondrial translation system is essential for energy production and defects result in severe, phenotypically diverse diseases, including mitochondrial diseases that typically affect postmitotic tissues with high metabolic demands. Understanding the complex mechanisms that underlie the pathologies of diseases involving impaired mitochondrial translation is key to tailoring specific treatments and effectively targeting the affected organs. Disease mutations have provided a fundamental, yet limited, understanding of mitochondrial protein synthesis, since effective modification of the mitochondrial genome has proven challenging. However, advances in next generation sequencing, cryoelectron microscopy, and multi-omic technologies have revealed unexpected and unusual features of the mitochondrial protein synthesis machinery in the last decade. Genome editing tools have generated unique models that have accelerated our mechanistic understanding of mitochondrial translation and its physiological importance. Here we review the most recent mouse models of disease pathogenesis caused by defects in mitochondrial protein synthesis and discuss their value for preclinical research and therapeutic development.

The genome sequence of the common awl robberfly, Neoitamus cyanurus (Loew, 1849)

We present a genome assembly from an individual female Neoitamus cyanurus (the common awl robberfly; Arthropoda; Insecta; Diptera; Asilidae). The genome sequence is 365.5 megabases in span. Most of the assembly is scaffolded into 10 chromosomal pseudomolecules. The mitochondrial genome has also been assembled and is 16.63 kilobases in length.

RNA degradation in human mitochondria: the journey is not finished.

Mitochondria are vital organelles present in almost all eukaryotic cells. Although most of the mitochondrial proteins are nuclear-encoded, mitochondria contain their own genome, whose proper expression is necessary for mitochondrial function. Transcription of the human mitochondrial genome results in the synthesis of long polycistronic transcripts that are subsequently processed by endonucleases to release individual RNA molecules, including precursors of sense protein-encoding mRNA (mt-mRNA) and a vast amount of antisense noncoding RNAs. Because of mitochondrial DNA (mtDNA) organization, the regulation of individual gene expression at the transcriptional level is limited. Although transcription of most protein-coding mitochondrial genes occurs with the same frequency, steady-state levels of mature transcripts are different. Therefore, post-transcriptional processes are important for regulating mt-mRNA levels. The mitochondrial degradosome is a complex composed of the RNA helicase SUV3 (also known as SUPV3L1) and polynucleotide phosphorylase (PNPase, PNPT1). It is the best-characterized RNA-degrading machinery in human mitochondria, which is primarily responsible for the decay of mitochondrial antisense RNA. The mechanism of mitochondrial sense RNA decay is less understood. This review aims to provide a general picture of mitochondrial genome expression, with a particular focus on mitochondrial RNA (mtRNA) degradation.

The genome sequence of the Grey Sedge caddis fly, Odontocerum albicorne (Scopoli, 1769).

We present a genome assembly from an individual male Odontocerum albicorne (the Grey Sedge caddis fly; Arthropoda; Insecta; Trichoptera; Odontoceridae). The genome sequence is 1,287.3 megabases in span. Most of the assembly is scaffolded into 31 chromosomal pseudomolecules, including the Z sex chromosome. The mitochondrial genome has also been assembled and is 16.57 kilobases in length.

The genome sequence of the silver stretch spider, Tetragnatha montana (Simon, 1874) (Araneae: Tetragnathidae)

We present a genome assembly from an individual female Tetragnatha montana (the silver stretch spider; Arthropoda; Arachnida; Araneae; Tetragnathidae). The genome sequence is 784.7 megabases in span. Most of the assembly is scaffolded into 13 chromosomal pseudomolecules, including the X sex chromosome. The mitochondrial genome has also been assembled and is 15.49 kilobases in length.

Coordinating mitochondrial translation with assembly of the OXPHOS complexes.

The mitochondrial oxidative phosphorylation (OXPHOS) system produces the majority of energy required by cells. Given the mitochondrion's endosymbiotic origin, the OXPHOS machinery is still under dual genetic control where most OXPHOS subunits are encoded by the nuclear DNA and imported into mitochondria, while a small subset is encoded on the mitochondrion's own genome, the mitochondrial DNA (mtDNA). The nuclear and mtDNA encoded subunits must be expressed and assembled in a highly orchestrated fashion to form a functional OXPHOS system and meanwhile prevent the generation of any harmful assembly intermediates. While several mechanisms have evolved in eukaryotes to achieve such a coordinated expression, this review will focus on how the translation of mtDNA encoded OXPHOS subunits is tailored to OXPHOS assembly.

MtDNA amplifies beryllium sulfate-induced inflammatory responses via the cGAS-STING pathway in 16HBE cells.

Beryllium sulfate (BeSO4) can cause inflammation through the mechanism, which has not been elucidated. Mitochondrial DNA (mtDNA) is a key contributor of inflammation. With mitochondrial damage, released mtDNA can bind to specific receptors (e.g., cGAS) and then activate related pathway to promote inflammatory responses. To investigate the mechanism of mtDNA in BeSO4-induced inflammatory response in 16HBE cells, we established the BeSO4-induced 16HBE cell inflammation model and the ethidium bromide (EB)-induced ρ016HBE cell model to detect the mtDNA content, oxidative stress-related markers, mitochondrial membrane potential, the expression of the cGAS-STING pathway, and inflammation-related factors. Our results showed that BeSO4 caused oxidative stress, decline of mitochondrial membrane potential, and the release of mtDNA into the cytoplasm of 16HBE cells. In addition, BeSO4 induced inflammation in 16HBE cells by activating the cGAS-STING pathway. Furthermore, mtDNA deletion inhibited the expression of cGAS-STING pathway, IL-10, TNF-α, and IFN-β. This study revealed a novel mechanism of BeSO4-induced inflammation in 16HBE cells, which contributes to the understanding of the molecular mechanism of beryllium and its compounds-induced toxicity.

Central dogma rates in human mitochondria.

In human cells, the nuclear and mitochondrial genomes engage in a complex interplay to produce dual-encoded oxidative phosphorylation (OXPHOS) complexes. The coordination of these dynamic gene expression processes is essential for producing matched amounts of OXPHOS protein subunits. This review focuses on our current understanding of the mitochondrial central dogma rates, highlighting the striking differences in gene expression rates between mitochondrial and nuclear genes. We synthesize a coherent model of mitochondrial gene expression kinetics, highlighting the emerging principles and emphasizing where more precise measurements would be beneficial. Such an understanding is pivotal for grasping the unique aspects of mitochondrial function and its role in cellular energetics, and it has profound implications for aging, metabolic disorders, and neurodegenerative diseases.

De Novo Assembly and Comparative Analysis of Mitochondrial Genomes of Two Pueraria montana Varieties

Pueraria montana is a species with important medicinal value and a complex genetic background. In this study, we sequenced and assembled the mitochondrial (mt) genomes of two varieties of P. montana. The mt genome lengths of P. montana var. thomsonii and P. montana var. montana were 457,390 bp and 456,731 bp, respectively. Both P. montana mitogenomes showed a multi-branched structure consisting of two circular molecules, with 56 genes annotated, comprising 33 protein-coding genes, 18 tRNA genes (trnC-GCA and trnM-CAU are multi-copy genes), and 3 rRNA genes. Then, 207 pairs of long repeats and 96 simple sequence repeats (SSRs) were detected in the mt genomes of P. montana, and 484 potential RNA-editing sites were found across the 33 mitochondrial protein-coding genes of each variety. Additionally, a syntenic sequence analysis showed a high collinearity between the two mt genomes. This work is the first to analyze the mt genomes of P. montana. It can provide information that can be used to analyze the structure of mt genomes of higher plants and provide a foundation for future comparative genomic studies and evolutionary biology research in related species.

Tools for editing the mammalian mitochondrial genome.

The manipulation of animal mitochondrial genomes has long been a challenge due to the lack of an effective transformation method. With the discovery of specific gene editing enzymes, designed to target pathogenic mitochondrial DNA mutations (often heteroplasmic), the selective removal or modification of mutant variants has become a reality. Because mitochondria cannot efficiently import RNAs, CRISPR has not been the first choice for editing mitochondrial genes. However, the last few years witnessed an explosion in novel and optimized non-CRISPR approaches to promote double-strand breaks or base-edit of mtDNA in vivo. Engineered forms of specific nucleases and cytidine/adenine deaminases form the basis for these techniques. I will review the newest developments that constitute the current toolbox for animal mtDNA gene editing in vivo, bringing these approaches not only to the exploration of mitochondrial function, but also closer to clinical use.

Sequence comparison of the mitochondrial genomes of Plesionika species (Caridea: Pandalidae), gene rearrangement and phylogenetic relationships of Caridea.

Despite the Caridean shrimps' vast species richness and ecological diversity, controversies persist in their molecular classification. Within Caridea, the Pandalidae family exemplifies significant taxonomic diversity. As of June 25, 2023, GenBank hosts only nine complete mitochondrial genomes (mitogenomes) for this family. The Plesionika genus within Pandalidae is recognized as polyphyletic. To improve our understanding of the mitogenome evolution and phylogenetic relationships of Caridea, this study introduces three novel mitogenome sequences from the Plesionika genus: P. ortmanni, P. izumiae and P. lophotes. The complete mitochondrial genomes of three Plesionika species were sequenced utilizing Illumina's next-generation sequencing (NGS) technology. After assembling and annotating the mitogenomes, we conducted structural analyses to examine circular maps, sequence structure characteristics, base composition, amino acid content, and synonymous codon usage frequency. Additionally, phylogenetic analysis was performed by integrating existing mitogenome sequences of true shrimp available in GenBank. The complete mitogenomes of the three Plesionika species encompass 37 canonical genes, comprising 13 protein-coding genes (PCGs), 22 transfer RNAs (tRNAs), two ribosomal RNAs (rRNAs), and one control region (CR). The lengths of these mitogenomes are as follows: 15,908 bp for P. ortmanni, 16,074 bp for P. izumiae and 15,933 bp for P. lophotes. Our analyses extended to their genomic features and structural functions, detailing base composition, gene arrangement, and codon usage. Additionally, we performed selection pressure analysis on the PCGs of all Pandalidae species available in Genbank, indicating evolutionary purification selection acted on the PCGs across Pandalidae species. Compared with the ancestral Caridea, translocation of two tRNA genes, i.e., trnP or trnT, were found in the two newly sequenced Plesionika species-P. izumiae and P. lophotes. We constructed a phylogenetic tree of Caridea using the sequences of 13 PCGs in mitogenomes. The results revealed that family Pandalidae exhibited robust monophyly, while genus Plesionika appeared to be a polyphyletic group. Gene rearrangements within the Pandalidae family were observed for the first time. Furthermore, a significant correlation was discovered between phylogenetics of the Caridea clade and arrangement of mitochondrial genes. Our findings offer a detailed exploration of Plesionika mitogenomes, laying a crucial groundwork for subsequent investigations into genetic diversity, phylogenetic evolution, and selective breeding within this genus.