scholarly journals Mitogenome Analysis of Four Lamiinae Species (Coleoptera: Cerambycidae) and Gene Expression Responses by Monochamus alternatus When Infected with the Parasitic Nematode, Bursaphelenchus mucronatus

Insects ◽  
2021 ◽  
Vol 12 (5) ◽  
pp. 453
Author(s):  
Zi-Yi Zhang ◽  
Jia-Yin Guan ◽  
Yu-Rou Cao ◽  
Xin-Yi Dai ◽  
Kenneth B. Storey ◽  
...  

We determined the mitochondrial gene sequence of Monochamus alternatus and three other mitogenomes of Lamiinae (Insect: Coleoptera: Cerambycidae) belonging to three genera (Aulaconotus, Apriona and Paraglenea) to enrich the mitochondrial genome database of Lamiinae and further explore the phylogenetic relationships within the subfamily. Phylogenetic trees of the Lamiinae were built using the Bayesian inference (BI) and maximum likelihood (ML) methods and the monophyly of Monochamus, Anoplophora, and Batocera genera was supported. Anoplophora chinensis, An. glabripennis and Aristobia reticulator were closely related, suggesting they may also be potential vectors for the transmission of the pine wood pathogenic nematode (Bursaphelenchus xylophilus) in addition to M. alternatus, a well-known vector of pine wilt disease. There is a special symbiotic relationship between M. alternatus and Bursaphelenchus xylophilus. As the native sympatric sibling species of B. xylophilus, B. mucronatus also has a specific relationship that is often overlooked. The analysis of mitochondrial gene expression aimed to explore the effect of B. mucronatus on the energy metabolism of the respiratory chain of M. alternatus adults. Using RT-qPCR, we determined and analyzed the expression of eight mitochondrial protein-coding genes (COI, COII, COIII, ND1, ND4, ND5, ATP6, and Cty b) between M. alternatus infected by B. mucronatus and M. alternatus without the nematode. Expression of all the eight mitochondrial genes were up-regulated, particularly the ND4 and ND5 gene, which were up-regulated by 4–5-fold (p < 0.01). Since longicorn beetles have immune responses to nematodes, we believe that their relationship should not be viewed as symbiotic, but classed as parasitic.

Forests ◽  
2022 ◽  
Vol 13 (1) ◽  
pp. 114
Author(s):  
Yang Wang ◽  
Mingxia Jin ◽  
Lichao Wang ◽  
Ailin Yu ◽  
Guai Xie ◽  
...  

In order to study the key gene in internal causes of pinewood nematode (PWN), Bursaphelenchus xylophilus, a departure from its vector beetle, Monochamus alternatus, we collected PWNs extracted from newly emerged M. alternatus and beetles 7 days after emergence. The total RNAs of the two groups of PWNs were extracted, transcriptomes sequencing was performed, and gene expression differences between the two groups of PWN were analyzed. It was found that the expression of the choline-phosphate cytidylyltransferase gene (pcyt-1) was markedly up-regulated. After inhibition of pcyt-1 expression by RNA interference, the rate of lipid degradation in PWN decreased significantly, and the motility of PWN also decreased significantly. The analysis identified that phosphatidylcholine could promote the emulsification and degradation of neutral lipid granules in PWN, which provides sufficient energy for PWN departure from M. alternatus. The up-regulation of the gene pcyt-1 is an important internal factor for PWN departure from its vector.


2020 ◽  
Vol 21 (11) ◽  
pp. 3820 ◽  
Author(s):  
Jia Xin Tang ◽  
Kyle Thompson ◽  
Robert W. Taylor ◽  
Monika Oláhová

The assembly of mitochondrial oxidative phosphorylation (OXPHOS) complexes is an intricate process, which—given their dual-genetic control—requires tight co-regulation of two evolutionarily distinct gene expression machineries. Moreover, fine-tuning protein synthesis to the nascent assembly of OXPHOS complexes requires regulatory mechanisms such as translational plasticity and translational activators that can coordinate mitochondrial translation with the import of nuclear-encoded mitochondrial proteins. The intricacy of OXPHOS complex biogenesis is further evidenced by the requirement of many tightly orchestrated steps and ancillary factors. Early-stage ancillary chaperones have essential roles in coordinating OXPHOS assembly, whilst late-stage assembly factors—also known as the LYRM (leucine–tyrosine–arginine motif) proteins—together with the mitochondrial acyl carrier protein (ACP)—regulate the incorporation and activation of late-incorporating OXPHOS subunits and/or co-factors. In this review, we describe recent discoveries providing insights into the mechanisms required for optimal OXPHOS biogenesis, including the coordination of mitochondrial gene expression with the availability of nuclear-encoded factors entering via mitochondrial protein import systems.


Nematology ◽  
2003 ◽  
Vol 5 (6) ◽  
pp. 843-849 ◽  
Author(s):  
Shota Jikumaru ◽  
Katsumi Togashi

Abstract Bursaphelenchus mucronatus is closely related to Bursaphelenchus xylophilus, the causative agent of pine wilt disease. Both nematodes are transmitted between host pine trees as the fourth-stage dispersal juveniles (JIV) by insect vectors. After the invasion of Japan by B. xylophilus, B. mucronatus, native to Japan, appears to have been replaced in the pine forests during the spread of the disease. To help understand this species replacement, the number of JIV carried by an insect vector (the initial nematode load) was compared between the two nematode species by using the beetle, Monochamus alternatus, in the laboratory. The initial load of B. mucronatus was significantly smaller than that of B. xylophilus although the number of third-stage dispersal juveniles (JIII) concentrated at the pupal chambers did not differ. Statistical analysis showed that the proportion of JIII moulting to JIV was the most important among three components explaining the difference in the initial load of B. mucronatus while the number of JIII concentrated at the pupal chamber was the most important for B. xylophilus. The phoretic affinity between the nematode and its vector is discussed in relation to its role in the species replacement.


F1000Research ◽  
2019 ◽  
Vol 8 ◽  
pp. 464 ◽  
Author(s):  
Leos G. Kral ◽  
Sara Watson

Background: Mitochondrial DNA of vertebrates contains genes for 13 proteins involved in oxidative phosphorylation. Some of these genes have been shown to undergo adaptive evolution in a variety of species. This study examines all mitochondrial protein coding genes in 11 darter species to determine if any of these genes show evidence of positive selection. Methods: The mitogenome from four darter was sequenced and annotated. Mitogenome sequences for another seven species were obtained from GenBank. Alignments of each of the protein coding genes were subject to codon-based identification of positive selection by Selecton, MEME and FEL. Results: Evidence of positive selection was obtained for six of the genes by at least one of the methods. CYTB was identified as having evolved under positive selection by all three methods at the same codon location. Conclusions: Given the evidence for positive selection of mitochondrial protein coding genes in darters, a more extensive analysis of mitochondrial gene evolution in all the extant darter species is warranted.


2018 ◽  
Vol 5 (5) ◽  
pp. 171900 ◽  
Author(s):  
Carolina Torres-Gutierrez ◽  
Tatiane M. P. de Oliveira ◽  
Kevin J. Emerson ◽  
Eduardo Sterlino Bergo ◽  
Maria Anice Mureb Sallum

The subgenus Melanoconion of the mosquito genus Culex is taxonomically diverse and is widely distributed in the Neotropical Region, with 10 species occurring in the Nearctic Region. Species of this subgenus pose a taxonomical challenge because morphological identification is based largely on anatomical characters of the male genitalia. We addressed the monophyly of the Spissipes and Melanoconion Sections of the subgenus Melanoconion and some of the informal groups in each section. Our sample taxa included 97 specimens representing 43 species, from which we analysed fragments of two single-copy nuclear genes ( CAD , HB ) and one mitochondrial gene ( COI ). Phylogenetic relationships within the subgenus are presented based on results of maximum-likelihood and Bayesian analyses using a multi-locus matrix of DNA sequences. We show a molecular phylogeny of Melanoconion in which both sections were recovered as monophyletic groups. The monophyly of the Atratus and Pilosus groups was confirmed. Within each section, other monophyletic groups were recovered highlighting the potential need for future nomenclature rearrangement. The phylogenetic signal contained in nuclear genes, when analysed together, was more informative than each gene analysed separately, corroborating monophyly of Melanoconion relative to Culex ( Culex ) species included in the analyses, the Melanoconion and Spissipes Sections and some species groups. Our results provide new information for the classification of the subgenus and additional data that can be used to improve species identification when a more representative taxon sampling is available.


2017 ◽  
Vol 41 (S1) ◽  
pp. S464-S464
Author(s):  
S. Hina

Neuroblastoma is a solid neuroendocrine tumour and most common type of cancer of infancy. It is a complex heterogeneous disease and many factors such as molecular, cellular and genetic features are involved in its development. Mitochondria play a pivotal role in neuronal cell survival or death. Neurons are highly reliant on aerobic oxidative phosphorylation (OXPHOS) for their energy needs. Defective activities of mitochondrial complexes I, II, III and IV have been identified in many neurological and neurodegenerative diseases. Human mitochondria with its own genetic material meet the needs required for the assembly of subunits of the oxidative phosphorylation (OXPHOS) complexes. A number of translational inhibitors are known that could potentially effect translation of mitochondrial protein synthesis. Among these puromycin, homoharringtonine and cyclohexamide were selected for the present study. The effect of these translational inhibitors on mitochondrial gene expression for the treatment of neuroblastoma are not well established. Therefore, in this study, we have investigated the effects of these translational inhibitors on the expression of human mitochondrial gene expression in SH-SY5Y neuroblastoma cells.We observed a significant effect on the level of mitochondrial transcripts upon exposure to these translation inhibitors in SH-SY5Y cells, however, the effects on expression of mitochondrial proteins were minimal. This suggests that translational inhibitors might not directly affect the abundance of mitochondrial proteins. Translational inhibitors induce significant effect on mitochondrial gene expression that can be lead to the new-targeted therapy for treating neuroblastoma.


Cells ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 1475 ◽  
Author(s):  
Rui Song ◽  
Xiang-Qun Hu ◽  
Lubo Zhang

MicroRNAs (miRNAs) are small noncoding RNAs functioning as crucial post-transcriptional regulators of gene expression involved in cardiovascular development and health. Recently, mitochondrial miRNAs (mitomiRs) have been shown to modulate the translational activity of the mitochondrial genome and regulating mitochondrial protein expression and function. Although mitochondria have been verified to be essential for the development and as a therapeutic target for cardiovascular diseases, we are just beginning to understand the roles of mitomiRs in the regulation of crucial biological processes, including energy metabolism, oxidative stress, inflammation, and apoptosis. In this review, we summarize recent findings regarding how mitomiRs impact on mitochondrial gene expression and mitochondrial function, which may help us better understand the contribution of mitomiRs to both the regulation of cardiovascular function under physiological conditions and the pathogenesis of cardiovascular diseases.


2010 ◽  
Vol 21 (8) ◽  
pp. 1315-1323 ◽  
Author(s):  
Florin Sasarman ◽  
Catherine Brunel-Guitton ◽  
Hana Antonicka ◽  
Timothy Wai ◽  
Eric A. Shoubridge ◽  
...  

Mutations in LRPPRC are responsible for the French Canadian variant of Leigh syndrome (LSFC), a neurodegenerative disorder caused by a tissue-specific deficiency in cytochrome c oxidase (COX). To investigate the pathogenic mechanism of disease, we studied LRPPRC function in LSFC and control fibroblasts. The level of mutated LRPPRC is reduced in LSFC cells, and this results in decreased steady-state levels of most mitochondrial mRNAs, but not rRNAs or tRNAs, a phenotype that can be reproduced by siRNA-mediated knockdown of LRPPRC in control cells. Processing of the primary transcripts appears normal. The resultant defect in mitochondrial protein synthesis in LSFC cells disproportionately affects the COX subunits, leading to an isolated COX assembly defect. Further knockdown of LRPPRC produces a generalized assembly defect in all oxidative phosphorylation complexes containing mtDNA-encoded subunits, due to a severe decrease in all mitochondrial mRNAs. LRPPRC exists in a high-molecular-weight complex, and it coimmunoprecipitates with SLIRP, a stem-loop RNA-binding protein. Although this interaction does not depend on mitochondrial mRNA, both proteins show reduced stability in its absence. These results implicate LRPPRC in posttranscriptional mitochondrial gene expression as part of a ribonucleoprotein complex that regulates the stability and handling of mature mRNAs.


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