Tissue-specific expression atlas of murine mitochondrial tRNAs

He, Qiufen; He, Xiao; Xiao, Yun; Zhao, Qiong; Ye, Zhenzhen; Cui, Limei; Chen, Ye; Guan, Min‐Xin

doi:10.1016/j.jbc.2021.100960

Cited by 17 publications

(7 citation statements)

References 51 publications

(95 reference statements)

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“…These observations could reflect intrinsic differences in tRNA modifying enzyme activity. Variations to canonical and modified ribonucleoside abundance could also indicate changes in tRNA expression levels [ 36 – 38 ]. Here, total nucleic acid was analyzed via PAGE, and bands representing tRNA or multiple tRNA species were seemingly differentially abundant between the examined cell types ( Supplementary Fig.…”

Section: Resultsmentioning

confidence: 99%

Ribonucleosides from tRNA in hyperglycemic mammalian cells and diabetic murine cardiac models

et al. 2023

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Section: Resultsmentioning

confidence: 99%

Ribonucleosides from tRNA in hyperglycemic mammalian cells and diabetic murine cardiac models

et al. 2023

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“…Blots were analyzed using a Typhoon FLA 9000 scanner and the ImageQuant TL software (GE Healthcare). The following probes were used for Northern hybridization [ 18 ] :…”

Section: Methodsmentioning

confidence: 99%

mt-tRNAs in the polymerase gamma mutant heart

Bayazit,

Francois,

McGrail

et al. 2023

J Cardiovasc Aging

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Introduction: Mice harboring a D257A mutation in the proofreading domain of the mitochondrial DNA polymerase, Polymerase Gamma (POLG), experience severe metabolic dysfunction and display hallmarks of accelerated aging. We previously reported a mitochondrial unfolded protein response (UPTmt) - like (UPRmt-like) gene and protein expression pattern in the right ventricular tissue of POLG mutant mice. Aim: We sought to determine if POLG mutation altered the expression of genes encoded by the mitochondria in a way that might also reduce proteotoxic stress. Methods and Results: The expression of genes encoded by the mitochondrial DNA was interrogated via RNA-seq and northern blot analysis. A striking, location-dependent effect was seen in the expression of mitochondrial-encoded tRNAs in the POLG mutant as assayed by RNA-seq. These expression changes were negatively correlated with the tRNA partner amino acid’s amyloidogenic potential. Direct measurement by northern blot was conducted on candidate mt-tRNAs identified from the RNA-seq. This analysis confirmed reduced expression of MT-TY in the POLG mutant but failed to show increased expression of MT-TP, which was dramatically increased in the RNA-seq data. Conclusion: We conclude that reduced expression of amyloid-associated mt-tRNAs is another indication of adaptive response to severe mitochondrial dysfunction in the POLG mutant. Incongruence between RNA-seq and northern blot measurement of MT-TP expression points towards the existence of mt-tRNA post-transcriptional modification regulation in the POLG mutant that alters either polyA capture or cDNA synthesis in RNA-seq library generation. Together, these data suggest that 1) evolution has distributed mt-tRNAs across the circular mitochondrial genome to allow chromosomal location-dependent mt-tRNA regulation (either by expression or PTM) and 2) this regulation is cognizant of the tRNA partner amino acid’s amyloidogenic properties.

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“…Other causes of heterogeneity can be cell- and tissue-specific differences in mitochondrial ncRNAs and proteins. 52 This review summarizes the heterogeneous characteristics of mitochondria in the pathological conditions of different tissues.…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial heterogeneity in diseases

Chen,

Zhou,

et al. 2023

Sig Transduct Target Ther

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As key organelles involved in cellular metabolism, mitochondria frequently undergo adaptive changes in morphology, components and functions in response to various environmental stresses and cellular demands. Previous studies of mitochondria research have gradually evolved, from focusing on morphological change analysis to systematic multiomics, thereby revealing the mitochondrial variation between cells or within the mitochondrial population within a single cell. The phenomenon of mitochondrial variation features is defined as mitochondrial heterogeneity. Moreover, mitochondrial heterogeneity has been reported to influence a variety of physiological processes, including tissue homeostasis, tissue repair, immunoregulation, and tumor progression. Here, we comprehensively review the mitochondrial heterogeneity in different tissues under pathological states, involving variant features of mitochondrial DNA, RNA, protein and lipid components. Then, the mechanisms that contribute to mitochondrial heterogeneity are also summarized, such as the mutation of the mitochondrial genome and the import of mitochondrial proteins that result in the heterogeneity of mitochondrial DNA and protein components. Additionally, multiple perspectives are investigated to better comprehend the mysteries of mitochondrial heterogeneity between cells. Finally, we summarize the prospective mitochondrial heterogeneity-targeting therapies in terms of alleviating mitochondrial oxidative damage, reducing mitochondrial carbon stress and enhancing mitochondrial biogenesis to relieve various pathological conditions. The possibility of recent technological advances in targeted mitochondrial gene editing is also discussed.

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Tissue-specific expression atlas of murine mitochondrial tRNAs

Cited by 17 publications

References 51 publications

Ribonucleosides from tRNA in hyperglycemic mammalian cells and diabetic murine cardiac models

Ribonucleosides from tRNA in hyperglycemic mammalian cells and diabetic murine cardiac models

mt-tRNAs in the polymerase gamma mutant heart

Mitochondrial heterogeneity in diseases

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