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Amino acids biosynthesis and nitrogen assimilation pathways: a great genomic deletion during eukaryotes evolution
BACKGROUND: Besides being building blocks for proteins, amino acids are also key metabolic intermediates in living cells. Surprisingly a variety of organisms are incapable of synthesizing some of them, thus named Essential Amino Acids (EAAs). How certain ancestral organisms successfully competed for...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3287585/ https://www.ncbi.nlm.nih.gov/pubmed/22369087 http://dx.doi.org/10.1186/1471-2164-12-S4-S2 |
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author | Guedes, RLM Prosdocimi, F Fernandes, GR Moura, LK Ribeiro, HAL Ortega, JM |
author_facet | Guedes, RLM Prosdocimi, F Fernandes, GR Moura, LK Ribeiro, HAL Ortega, JM |
author_sort | Guedes, RLM |
collection | PubMed |
description | BACKGROUND: Besides being building blocks for proteins, amino acids are also key metabolic intermediates in living cells. Surprisingly a variety of organisms are incapable of synthesizing some of them, thus named Essential Amino Acids (EAAs). How certain ancestral organisms successfully competed for survival after losing key genes involved in amino acids anabolism remains an open question. Comparative genomics searches on current protein databases including sequences from both complete and incomplete genomes among diverse taxonomic groups help us to understand amino acids auxotrophy distribution. RESULTS: Here, we applied a methodology based on clustering of homologous genes to seed sequences from autotrophic organisms Saccharomyces cerevisiae (yeast) and Arabidopsis thaliana (plant). Thus we depict evidences of presence/absence of EAA biosynthetic and nitrogen assimilation enzymes at phyla level. Results show broad loss of the phenotype of EAAs biosynthesis in several groups of eukaryotes, followed by multiple secondary gene losses. A subsequent inability for nitrogen assimilation is observed in derived metazoans. CONCLUSIONS: A Great Deletion model is proposed here as a broad phenomenon generating the phenotype of amino acids essentiality followed, in metazoans, by organic nitrogen dependency. This phenomenon is probably associated to a relaxed selective pressure conferred by heterotrophy and, taking advantage of available homologous clustering tools, a complete and updated picture of it is provided. |
format | Online Article Text |
id | pubmed-3287585 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-32875852012-02-28 Amino acids biosynthesis and nitrogen assimilation pathways: a great genomic deletion during eukaryotes evolution Guedes, RLM Prosdocimi, F Fernandes, GR Moura, LK Ribeiro, HAL Ortega, JM BMC Genomics Proceedings BACKGROUND: Besides being building blocks for proteins, amino acids are also key metabolic intermediates in living cells. Surprisingly a variety of organisms are incapable of synthesizing some of them, thus named Essential Amino Acids (EAAs). How certain ancestral organisms successfully competed for survival after losing key genes involved in amino acids anabolism remains an open question. Comparative genomics searches on current protein databases including sequences from both complete and incomplete genomes among diverse taxonomic groups help us to understand amino acids auxotrophy distribution. RESULTS: Here, we applied a methodology based on clustering of homologous genes to seed sequences from autotrophic organisms Saccharomyces cerevisiae (yeast) and Arabidopsis thaliana (plant). Thus we depict evidences of presence/absence of EAA biosynthetic and nitrogen assimilation enzymes at phyla level. Results show broad loss of the phenotype of EAAs biosynthesis in several groups of eukaryotes, followed by multiple secondary gene losses. A subsequent inability for nitrogen assimilation is observed in derived metazoans. CONCLUSIONS: A Great Deletion model is proposed here as a broad phenomenon generating the phenotype of amino acids essentiality followed, in metazoans, by organic nitrogen dependency. This phenomenon is probably associated to a relaxed selective pressure conferred by heterotrophy and, taking advantage of available homologous clustering tools, a complete and updated picture of it is provided. BioMed Central 2011-12-22 /pmc/articles/PMC3287585/ /pubmed/22369087 http://dx.doi.org/10.1186/1471-2164-12-S4-S2 Text en Copyright ©2011 Guedes et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Proceedings Guedes, RLM Prosdocimi, F Fernandes, GR Moura, LK Ribeiro, HAL Ortega, JM Amino acids biosynthesis and nitrogen assimilation pathways: a great genomic deletion during eukaryotes evolution |
title | Amino acids biosynthesis and nitrogen assimilation pathways: a great genomic deletion during eukaryotes evolution |
title_full | Amino acids biosynthesis and nitrogen assimilation pathways: a great genomic deletion during eukaryotes evolution |
title_fullStr | Amino acids biosynthesis and nitrogen assimilation pathways: a great genomic deletion during eukaryotes evolution |
title_full_unstemmed | Amino acids biosynthesis and nitrogen assimilation pathways: a great genomic deletion during eukaryotes evolution |
title_short | Amino acids biosynthesis and nitrogen assimilation pathways: a great genomic deletion during eukaryotes evolution |
title_sort | amino acids biosynthesis and nitrogen assimilation pathways: a great genomic deletion during eukaryotes evolution |
topic | Proceedings |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3287585/ https://www.ncbi.nlm.nih.gov/pubmed/22369087 http://dx.doi.org/10.1186/1471-2164-12-S4-S2 |
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