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Abstract-With the rapid development of new and innovative applications for mobile devices like smartphones, advances in battery technology have not kept pace with rapidly growing energy demands. Thus energy consumption has become a more and more important issue of mobile devices. To meet the requirements of saving energy, it is critical to monitor and analyze the energy consumption of applications on smartphones. For this purpose, we develop a smart energy monitoring system called SEMO for smartphones using Android operating system. It can profile mobile applications with battery usage information, which is vital for both developers and users.

While N6-methyldeoxyadenine (6mA) modification has been linked to fundamental regulatory processes in prokaryotes, its prevalence and functional implications in eukaryotes are controversial. Here, we report 6mA-Sniper to quantify 6mA sites in eukaryotes at single-nucleotide resolution. With 6mA-Sniper, we delineated an accurate 6mA profile in C. elegans with 2,034 sites, significantly enriched on sequences of [GC]GAG motif. Twenty-six of 39 6mA events with MnlI restriction endonuclease sites were experimentally verified, demonstrating the feasibility of this method. Notably, the enrichment of these 6mA sites on a specific sequence motif, their within-population conservation and the combinatorial patterns, and the selective constrains on them jointly support an active model for the shaping of the profile by some undiscovered methyltransferases. We then report the dominant contribution of one new methyltransferase, METL-9, in shaping the base level and the stress-dependent changes of 6mA profile in C. elegans, in that the levels of 6mAs at single-nucleotide resolution are significantly decreased in strains with the removal of METL-9 (METL-9 KO-OP50), while generally increased after P. aeruginosa infection. Accordingly, we identified 998 stress-dependent 6mA sites emerged specifically after the infection, enriched in stimulus response genes generally upregulated after the infection. The upregulation of these genes is likely regulated through a mutual exclusive crosstalk between 6mA and H3K27me3 modification, as supported by their cooccurrence, and the increasing of H3K27me3 at regions marked by decreased 6mA levels in METL-9 KO-OP50 strains. Notably, in different C. elegans strains, the cross-strain genetic variants removing 6mA sites are associated with the decreased expression of their host genes, and the removal of two randomly-selected 6mA events with genome editing directly decreased the expression of their host genes. We thus highlight 6mA regulation as a previously-neglected regulator of eukaryote transcriptomes in stress response.