Differential regulation of the Tor gene homolog drives the red/green pigmentation phenotype in the aphid Myzus persicae.

In some aphid species, intraspecific variation in body colour is caused by differential carotenoid content: whilst green aphids contain only yellow carotenoids (β-, γ-, and β,γ-carotenes), red aphids additionally possess red carotenoids (torulene and 3,4-didehydrolycopene). Unusually, within animals who typically obtain carotenoids from their diet, ancestral horizontal gene transfer of carotenoid biosynthetic genes from fungi (followed by gene duplication), have imbued aphids with the intrinsic gene repertoire necessary to biosynthesise carotenoids. In the pea aphid, Acyrthosiphon pisum a lycopene (phytoene) desaturase gene (Tor) underpins the red/green phenotype, with this locus present in heterozygous form in red individuals but absent in green aphids, resulting in them being unable to convert lycopene into the red compounds 3,4-didehydrolycopene and torulene. The green peach aphid, Myzus persicae, separated from the pea aphid for ≈45MY also exists as distinct colour variable morphs, with both red and green individuals present. Here, we examined genomic data for both red and green morphs of M. persicae and identified an enlarged (compared to A. pisum) repertoire of 16 carotenoid biosynthetic genes (11 carotenoid desaturases and five carotenoid cyclase/synthase genes). From these, we identify the homolog of A. pisum Tor (here called carotene desaturase 2 or CDE-2) and show through 3D modelling that this homolog can accommodate the torulene precursor lycopene and, through RNA knockdown feeding experiments, demonstrate that disabling CDE-2 expression in red M. persicae clones results in green-coloured offspring. Unlike in A. pisum, we show that functional CDE-2 is present in the genomes of both red and green aphids. However, expression differences between the two colour morphs (350-700 fold CDE-2 overexpression in red clones), potentially driven by variants identified in upstream putative regulatory elements, underpin this phenotype. Thus, whilst aphids have a common origin of their carotenoid biosynthetic pathway, two aphid species separated for over 40MY have evolved very different drivers of intraspecific colour variation

The genetic architecture of a host shift: An adaptive walk protected an aphid and its endosymbiont from plant chemical defenses

This is the final version. Available from American Association for the Advancement of Science via the DOI in this record. The RNA and DNA sequence data generated in this study have been deposited with NCBI under accession number PRJNA574571. The sequence of RPS11/ADAMTS9 has been deposited under NCBI accession number MF1555663, and the accession numbers of other genes characterized in this study can be found in data file S1. All other data needed to evaluate the conclusions in the paper are present in the paper and/or the Supplementary Materials. Additional data related to this paper may be requested from the authors.Host shifts can lead to ecological speciation and the emergence of new pests and pathogens. However, the mutational events that facilitate the exploitation of novel hosts are poorly understood. Here, we characterize an adaptive walk underpinning the host shift of the aphid Myzus persicae to tobacco, including evolution of mechanisms that overcame tobacco chemical defenses. A series of mutational events added as many as 1.5 million nucleotides to the genome of the tobacco-adapted subspecies, M. p. nicotianae, and yielded profound increases in expression of an enzyme that efficiently detoxifies nicotine, both in aphid gut tissue and in the bacteriocytes housing the obligate aphid symbiont Buchnera aphidicola. This dual evolutionary solution overcame the challenge of preserving fitness of a mutualistic symbiosis during adaptation to a toxic novel host. Our results reveal the intricate processes by which genetic novelty can arise and drive the evolution of key innovations required for ecological adaptation.European Union Horizon 2020Czech Science FoundationCzech Science FoundationEuropean Social Fund and the state budget of the Czech RepublicBiotechnology and Biological Sciences Research Council (BBSRC

Perhitungan Harga Pokok Produksi Pada Jamu Singkir Angin (Studi Kasus pada PT.Nyonya Meneer Semarang)

Penentuan harga pokok sangat penting bagi perusahaan karena mempengaruhi besarnya biaya yang dikeluarkan oleh perusahaan. Tujuan laporan perhitungan harga pokok produksi adalah untuk menetapkan harga jual, agar dapat menentukan biaya total dan biaya per unit dari pekerjaan yang diterima dari satu atau beberapa proses produksi lainnya, biaya total dan biaya per unit dari bahan baku, tenaga kerja, dan overhead pabrik yang ditambahkan oleh proses produksi tersebut. Berdasarkan uraian di atas, maka judul dalam penelitian ini adalah :“ Perhitungan Harga Pokok Produksi Pada Jamu Singkir Angin (Studi Kasus Pada PT. Nyonya Meneer Semarang)”. Tujuan dalam penelitian ini adalah mengetahui perhitungan harga pokok produksi pada Jamu Singkir Angin pada PT.Nyonya Meneer dan untuk mengetahui perbandingan perhitungan Harga Pokok Produksi Pada Jamu Singkir Angin pada PT.Nyonya Meneer dengan metode full costing. Data penelitian ini adalah data sekunder dengan menggunakan harga pokok produksi PT. Nyonya Meneer Semarang selama bulan Januari-Desember 2011. Metode analisis data yang digunakan adalah metode full costing. Hasil análisis adalah metode harga pokok produksi yang diterapkan di PT. Nonya Meneer menggunakan sistem biaya overhead pabrik variabel costing, yang belum memisahkan biaya overhead pabrik. Penelitian ini perhitungan harga pokok produksi menggunakan metode full costing, yang memisahkan biaya overhead pabrik variabel yang terdiri dari biaya bahan penolong, biaya lembur, biaya listrik, biaya bahan bakar, suplies pabrik dan biaya telepon dan biaya overhead pabrik tetap yang terdiri dari biaya tunjangan THR bonus, biaya pemeriharaan dan biaya depresiasi

The genetic architecture of a host shift: An adaptive walk protected an aphid and its endosymbiont from plant chemical defenses

Host shifts can lead to ecological speciation and the emergence of new pests and pathogens. However, the mutational events that facilitate the exploitation of novel hosts are poorly understood. Here, we characterize an adaptive walk underpinning the host shift of the aphid Myzus persicae to tobacco, including evolution of mechanisms that overcame tobacco chemical defenses. A series of mutational events added as many as 1.5 million nucleotides to the genome of the tobacco-adapted subspecies, M. p. nicotianae, and yielded profound increases in expression of an enzyme that efficiently detoxifies nicotine, both in aphid gut tissue and in the bacteriocytes housing the obligate aphid symbiont Buchnera aphidicola. This dual evolutionary solution overcame the challenge of preserving fitness of a mutualistic symbiosis during adaptation to a toxic novel host. Our results reveal the intricate processes by which genetic novelty can arise and drive the evolution of key innovations required for ecological adaptation