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The tissue specificity of mitochondrial tRNA mutations remains largely elusive. In this study, we demonstrated the deleterious effects of tRNA Thr 15927G>A mutation that contributed to pathogenesis of coronary artery disease. The m.15927G>A mutation abolished the highly conserved base-pairing (28C-42G) of anticodon stem of tRNA Thr . Using molecular dynamics simulations, we showed that the m.15927G>A mutation caused unstable tRNA Thr structure, supported by decreased melting temperature and slower electrophoretic mobility of mutated tRNA. Using cybrids constructed by transferring mitochondria from a Chinese family carrying the m.15927G>A mutation and a control into mitochondrial DNA (mtDNA)-less human umbilical vein endothelial cells, we demonstrated that the m.15927G>A mutation caused significantly decreased efficiency in aminoacylation and steady-state levels of tRNA Thr . The aberrant tRNA Thr metabolism yielded variable decreases in mtDNA-encoded polypeptides, respiratory deficiency, diminished membrane potential and increased the production of reactive oxygen species. The m.15927G>A mutation promoted the apoptosis, evidenced by elevated release of cytochrome c into cytosol and increased levels of apoptosis-activated proteins: caspases 3, 7, 9 and PARP. Moreover, the lower wound healing cells and perturbed tube formation were observed in mutant cybrids, indicating altered angiogenesis. Our findings provide new insights into the pathophysiology of coronary artery disease, which is manifested by tRNA Thr mutation-induced alterations.

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Abstract-We consider the scenario of distributed data aggregation in wireless sensor networks, where each sensor can obtain and estimate the information of the whole sensing field through local data exchange and aggregation. The intrinsic trade-off between energy and delay in aggregation operations imposes a crucial question on nodes to decide optimal instants for forwarding their samples. The samples could be composed of the information from their own sensor readings or an aggregation of information with other samples forwarded from neighboring nodes. By considering the randomness of the sample arrival instants and the uncertainty of the availability of the multiaccess communication channel due to the asynchronous nature of information exchange among neighboring nodes, we propose a decision process model to analyze this problem and determine the optimal decision policies at nodes with local information. We show that, once the statistics of the sample arrival and the availability of the channel satisfy certain conditions, there exist optimal control-limit type policies which are easy to implement in practice. In the case that the required conditions are not satisfied, we provide two learning algorithms to solve a finitestate approximation model of the decision problem. Simulations on a practical distributed data aggregation scenario demonstrate the effectiveness of the developed policies, which can also achieve a desired energy-delay tradeoff.

Defects in the posttranscriptional modifications of mitochondrial tRNAs have been linked to human diseases, but their pathophysiology remains elusive. In this report, we investigated the molecular mechanism underlying a deafness-associated tRNAIle 4295A>G mutation affecting a highly conserved adenosine at position 37, 3′ adjacent to the tRNA’s anticodon. Primer extension and methylation activity assays revealed that the m.4295A>G mutation introduced a tRNA methyltransferase 5 (TRMT5)-catalyzed m1G37 modification of tRNAIle. Molecular dynamics simulations suggested that the m.4295A>G mutation affected tRNAIle structure and function, supported by increased melting temperature, conformational changes and instability of mutated tRNA. An in vitro processing experiment revealed that the m.4295A>G mutation reduced the 5′ end processing efficiency of tRNAIle precursors, catalyzed by RNase P. We demonstrated that cybrid cell lines carrying the m.4295A>G mutation exhibited significant alterations in aminoacylation and steady-state levels of tRNAIle. The aberrant tRNA metabolism resulted in the impairment of mitochondrial translation, respiratory deficiency, decreasing membrane potentials and ATP production, increasing production of reactive oxygen species and promoting autophagy. These demonstrated the pleiotropic effects of m.4295A>G mutation on tRNAIle and mitochondrial functions. Our findings highlighted the essential role of deficient posttranscriptional modifications in the structure and function of tRNA and their pathogenic consequence of deafness.

Graphene is a hot star in materials science with various potential application aspects, including in Li‐ion battery and supercapacitor. The burst of scientific papers in this area seems to validate the performance of graphene, but also arouses large dispute. Herein, we share our judgment of these trends to all, encouraging the discussion and enhancing the understanding of the structure‐performance relationship of graphene.

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The study examined how a conversation partner’s gender and gender-language consistency influence communicators’ gender-based language (i.e., references to emotion and tentativeness) and gender identity salience. In an email exchange, an experiment manipulated an ostensible conversation partner’s gender and use of references to emotion in ways stereotypically consistent or inconsistent with the partner’s gender. The conversation partner’s gender and gender-language consistency affected communicators’ references to emotion in ways that generally confirmed hypotheses. Participants’ references to emotion were congruent with the conversation partner’s use of references to emotion regardless of participants’ own gender. Results pertaining to tentative language and gender salience demonstrated no substantive differences.