Usuária:Pwoli/Testes/Gene

Origem: Wikipédia, a enciclopédia livre.

Inheritance[editar | editar código-fonte]

Illustration of autosomal recessive inheritance. Each parent has one blue allele and one white allele. Each of their 4 children inherit one allele from each parent such that one child ends up with two blue alleles, one child has two white alleles and two children have one of each allele. Only the child with both blue alleles shows the trait because the trait is recessive.
Inheritance of a gene that has two different alleles (blue and white). The gene is located on an autosomal chromosome. The white allele is recessive to the blue allele. The probability of each outcome in the children's generation is one quarter, or 25 percent.
Ver artigos principais: Mendelian inheritance e Heredity

Organisms inherit their genes from their parents. Asexual organisms simply inherit a complete copy of their parent's genome. Sexual organisms have two copies of each chromosome because they inherit one complete set from each parent.[1]:1

Mendelian inheritance[editar | editar código-fonte]

According to Mendelian inheritance, variations in an organism's phenotype (observable physical and behavioral characteristics) are due in part to variations in its genotype (particular set of genes). Each gene specifies a particular trait with a different sequence of a gene (alleles) giving rise to different phenotypes. Most eukaryotic organisms (such as the pea plants Mendel worked on) have two alleles for each trait, one inherited from each parent.[1]:20

Alleles at a locus may be dominant or recessive; dominant alleles give rise to their corresponding phenotypes when paired with any other allele for the same trait, whereas recessive alleles give rise to their corresponding phenotype only when paired with another copy of the same allele. If you know the genotypes of the organisms, you can determine which alleles are dominant and which are recessive. For example, if the allele specifying tall stems in pea plants is dominant over the allele specifying short stems, then pea plants that inherit one tall allele from one parent and one short allele from the other parent will also have tall stems. Mendel's work demonstrated that alleles assort independently in the production of gametes, or germ cells, ensuring variation in the next generation. Although Mendelian inheritance remains a good model for many traits determined by single genes (including a number of well-known genetic disorders) it does not include the physical processes of DNA replication and cell division.[2][3]

DNA replication and cell division[editar | editar código-fonte]

The growth, development, and reproduction of organisms relies on cell division; the process by which a single cell divides into two usually identical daughter cells. This requires first making a duplicate copy of every gene in the genome in a process called DNA replication.[1]:5.2 The copies are made by specialized enzymes known as DNA polymerases, which "read" one strand of the double-helical DNA, known as the template strand, and synthesize a new complementary strand. Because the DNA double helix is held together by base pairing, the sequence of one strand completely specifies the sequence of its complement; hence only one strand needs to be read by the enzyme to produce a faithful copy. The process of DNA replication is semiconservative; that is, the copy of the genome inherited by each daughter cell contains one original and one newly synthesized strand of DNA.[1]:5.2

The rate of DNA replication in living cells was first measured as the rate of phage T4 DNA elongation in phage-infected E. coli and found to be impressively rapid.[4] During the period of exponential DNA increase at 37 °C, the rate of elongation was 749 nucleotides per second.

After DNA replication is complete, the cell must physically separate the two copies of the genome and divide into two distinct membrane-bound cells.[1]:18.2 In prokaryotes (bacteria and archaea) this usually occurs via a relatively simple process called binary fission, in which each circular genome attaches to the cell membrane and is separated into the daughter cells as the membrane invaginates to split the cytoplasm into two membrane-bound portions. Binary fission is extremely fast compared to the rates of cell division in eukaryotes. Eukaryotic cell division is a more complex process known as the cell cycle; DNA replication occurs during a phase of this cycle known as S phase, whereas the process of segregating chromosomes and splitting the cytoplasm occurs during M phase.[1]:18.1

Molecular inheritance[editar | editar código-fonte]

The duplication and transmission of genetic material from one generation of cells to the next is the basis for molecular inheritance and the link between the classical and molecular pictures of genes. Organisms inherit the characteristics of their parents because the cells of the offspring contain copies of the genes in their parents' cells. In asexually reproducing organisms, the offspring will be a genetic copy or clone of the parent organism. In sexually reproducing organisms, a specialized form of cell division called meiosis produces cells called gametes or germ cells that are haploid, or contain only one copy of each gene.[1]:20.2 The gametes produced by females are called eggs or ova, and those produced by males are called sperm. Two gametes fuse to form a diploid fertilized egg, a single cell that has two sets of genes, with one copy of each gene from the mother and one from the father.[1]:20

During the process of meiotic cell division, an event called genetic recombination or crossing-over can sometimes occur, in which a length of DNA on one chromatid is swapped with a length of DNA on the corresponding homologous non-sister chromatid. This can result in reassortment of otherwise linked alleles.[1]:5.5 The Mendelian principle of independent assortment asserts that each of a parent's two genes for each trait will sort independently into gametes; which allele an organism inherits for one trait is unrelated to which allele it inherits for another trait. This is in fact only true for genes that do not reside on the same chromosome or are located very far from one another on the same chromosome. The closer two genes lie on the same chromosome, the more closely they will be associated in gametes and the more often they will appear together (known as genetic linkage).[5] Genes that are very close are essentially never separated because it is extremely unlikely that a crossover point will occur between them.[5]

Molecular evolution[editar | editar código-fonte]

Ver artigo principal: Molecular evolution

Mutation[editar | editar código-fonte]

DNA replication is for the most part extremely accurate, however errors (mutations) do occur.[1]:7.6 The error rate in eukaryotic cells can be as low as 10−8 per nucleotide per replication,[6][7] whereas for some RNA viruses it can be as high as 10−3.[8] This means that each generation, each human genome accumulates 1–2 new mutations.[8] Small mutations can be caused by DNA replication and the aftermath of DNA damage and include point mutations in which a single base is altered and frameshift mutations in which a single base is inserted or deleted. Either of these mutations can change the gene by missense (change a codon to encode a different amino acid) or nonsense (a premature stop codon).[9] Larger mutations can be caused by errors in recombination to cause chromosomal abnormalities including the duplication, deletion, rearrangement or inversion of large sections of a chromosome. Additionally, DNA repair mechanisms can introduce mutational errors when repairing physical damage to the molecule. The repair, even with mutation, is more important to survival than restoring an exact copy, for example when repairing double-strand breaks.[1]:5.4

When multiple different alleles for a gene are present in a species's population it is called polymorphic. Most different alleles are functionally equivalent, however some alleles can give rise to different phenotypic traits. A gene's most common allele is called the wild type, and rare alleles are called mutants. The genetic variation in relative frequencies of different alleles in a population is due to both natural selection and genetic drift.[10] The wild-type allele is not necessarily the ancestor of less common alleles, nor is it necessarily fitter.

Most mutations within genes are neutral, having no effect on the organism's phenotype (silent mutations). Some mutations do not change the amino acid sequence because multiple codons encode the same amino acid (synonymous mutations). Other mutations can be neutral if they lead to amino acid sequence changes, but the protein still functions similarly with the new amino acid (e.g. conservative mutations). Many mutations, however, are deleterious or even lethal, and are removed from populations by natural selection. Genetic disorders are the result of deleterious mutations and can be due to spontaneous mutation in the affected individual, or can be inherited. Finally, a small fraction of mutations are beneficial, improving the organism's fitness and are extremely important for evolution, since their directional selection leads to adaptive evolution.[1]:7.6

Sequence homology[editar | editar código-fonte]

A sequence alignment, produced by ClustalO, of mammalian histone proteins

Genes with a most recent common ancestor, and thus a shared evolutionary ancestry, are known as homologs.[11] These genes appear either from gene duplication within an organism's genome, where they are known as paralogous genes, or are the result of divergence of the genes after a speciation event, where they are known as orthologous genes,[1]:7.6 and often perform the same or similar functions in related organisms. It is often assumed that the functions of orthologous genes are more similar than those of paralogous genes, although the difference is minimal.[12][13]

The relationship between genes can be measured by comparing the sequence alignment of their DNA.[1]:7.6 The degree of sequence similarity between homologous genes is called conserved sequence. Most changes to a gene's sequence do not affect its function and so genes accumulate mutations over time by neutral molecular evolution. Additionally, any selection on a gene will cause its sequence to diverge at a different rate. Genes under stabilizing selection are constrained and so change more slowly whereas genes under directional selection change sequence more rapidly.[14] The sequence differences between genes can be used for phylogenetic analyses to study how those genes have evolved and how the organisms they come from are related.[15][16]

Origins of new genes[editar | editar código-fonte]

Evolutionary fate of duplicate genes.

The most common source of new genes in eukaryotic lineages is gene duplication, which creates copy number variation of an existing gene in the genome.[17][18] The resulting genes (paralogs) may then diverge in sequence and in function. Sets of genes formed in this way compose a gene family. Gene duplications and losses within a family are common and represent a major source of evolutionary biodiversity.[19] Sometimes, gene duplication may result in a nonfunctional copy of a gene, or a functional copy may be subject to mutations that result in loss of function; such nonfunctional genes are called pseudogenes.[1]:7.6

"Orphan" genes, whose sequence shows no similarity to existing genes, are less common than gene duplicates. The human genome contains an estimate 18[20] to 60[21] genes with no identifiable homologs outside humans. Orphan genes arise primarily from either de novo emergence from previously non-coding sequence, or gene duplication followed by such rapid sequence change that the original relationship becomes undetectable.[22] De novo genes are typically shorter and simpler in structure than most eukaryotic genes, with few if any introns.[17] Over long evolutionary time periods, de novo gene birth may be responsible for a significant fraction of taxonomically-restricted gene families.[23]

Horizontal gene transfer refers to the transfer of genetic material through a mechanism other than reproduction. This mechanism is a common source of new genes in prokaryotes, sometimes thought to contribute more to genetic variation than gene duplication.[24] It is a common means of spreading antibiotic resistance, virulence, and adaptive metabolic functions.[25][26] Although horizontal gene transfer is rare in eukaryotes, likely examples have been identified of protist and alga genomes containing genes of bacterial origin.[27][28]

Genome[editar | editar código-fonte]

The genome is the total genetic material of an organism and includes both the genes and non-coding sequences.[29]

Number of genes[editar | editar código-fonte]

Depiction of numbers of genes for representative plants (green), vertebrates (blue), invertebrates (red), fungi (yellow), bacteria (purple), and viruses (grey). An inset on the right shows the smaller genomes expanded 100-fold area-wise.[30][31][32][33][34][35][36][37]

The genome size, and the number of genes it encodes varies widely between organisms. The smallest genomes occur in viruses,[38] and viroids (which act as a single non-coding RNA gene).[39] Conversely, plants can have extremely large genomes,[40] with rice containing >46,000 protein-coding genes.[34] The total number of protein-coding genes (the Earth's proteome) is estimated to be 5 million sequences.[41]

Although the number of base-pairs of DNA in the human genome has been known since the 1960s, the estimated number of genes has changed over time as definitions of genes, and methods of detecting them have been refined. Initial theoretical predictions of the number of human genes were as high as 2,000,000.[42] Early experimental measures indicated there to be 50,000–100,000 transcribed genes (expressed sequence tags).[43] Subsequently, the sequencing in the Human Genome Project indicated that many of these transcripts were alternative variants of the same genes, and the total number of protein-coding genes was revised down to ~20,000[37] with 13 genes encoded on the mitochondrial genome.[35] With the GENCODE annotation project, that estimate has continued to fall to 19,000.[44] Of the human genome, only 1–2% consists of protein-coding sequences,[45] with the remainder being 'noncoding' DNA such as introns, retrotransposons, and noncoding RNAs.[45][46] Every multicellular organism has all its genes in each cell of its body but not every gene functions in every cell .

Essential genes[editar | editar código-fonte]

Ver artigo principal: Essential gene
Gene functions in the minimal genome of the synthetic organism, Syn 3.[47]

Essential genes are the set of genes thought to be critical for an organism's survival.[48] This definition assumes the abundant availability of all relevant nutrients and the absence of environmental stress. Only a small portion of an organism's genes are essential. In bacteria, an estimated 250–400 genes are essential for Escherichia coli and Bacillus subtilis, which is less than 10% of their genes.[49][50][51] Half of these genes are orthologs in both organisms and are largely involved in protein synthesis.[51] In the budding yeast Saccharomyces cerevisiae the number of essential genes is slightly higher, at 1000 genes (~20% of their genes).[52] Although the number is more difficult to measure in higher eukaryotes, mice and humans are estimated to have around 2000 essential genes (~10% of their genes).[53] The synthetic organism, Syn 3, has a minimal genome of 473 essential genes and quasi-essential genes (necessary for fast growth), although 149 have unknown function.[47]

Essential genes include housekeeping genes (critical for basic cell functions)[54] as well as genes that are expressed at different times in the organisms development or life cycle.[55] Housekeeping genes are used as experimental controls when analysing gene expression, since they are constitutively expressed at a relatively constant level.

Genetic and genomic nomenclature[editar | editar código-fonte]

Gene nomenclature has been established by the HUGO Gene Nomenclature Committee (HGNC), a committee of the Human Genome Organisation, for each known human gene in the form of an approved gene name and symbol (short-form abbreviation), which can be accessed through a database maintained by HGNC. Symbols are chosen to be unique, and each gene has only one symbol (although approved symbols sometimes change). Symbols are preferably kept consistent with other members of a gene family and with homologs in other species, particularly the mouse due to its role as a common model organism.[56]

Genetic engineering[editar | editar código-fonte]

Comparison of conventional plant breeding with transgenic and cisgenic genetic modification.
Ver artigo principal: Genetic engineering

Genetic engineering is the modification of an organism's genome through biotechnology. Since the 1970s, a variety of techniques have been developed to specifically add, remove and edit genes in an organism.[57] Recently developed genome engineering techniques use engineered nuclease enzymes to create targeted DNA repair in a chromosome to either disrupt or edit a gene when the break is repaired.[58][59][60][61] The related term synthetic biology is sometimes used to refer to extensive genetic engineering of an organism.[62]

Genetic engineering is now a routine research tool with model organisms. For example, genes are easily added to bacteria[63] and lineages of knockout mice with a specific gene's function disrupted are used to investigate that gene's function.[64][65] Many organisms have been genetically modified for applications in agriculture, industrial biotechnology, and medicine.

For multicellular organisms, typically the embryo is engineered which grows into the adult genetically modified organism.[66] However, the genomes of cells in an adult organism can be edited using gene therapy techniques to treat genetic diseases.

See also[editar | editar código-fonte]

* Copy number variation

References[editar | editar código-fonte]

Citations[editar | editar código-fonte]

  1. ↑ a b c d e f g h i j k l m n o Erro de citação: Etiqueta <ref> inválida; não foi fornecido texto para as refs de nome MBOC
  2. ↑ Miko, Ilona (2008). «Gregor Mendel and the Principles of Inheritance». Nature Publishing Group. Nature Education Knowledge. SciTable. 1 (1): 134 
  3. ↑ Chial, Heidi (2008). «Mendelian Genetics: Patterns of Inheritance and Single-Gene Disorders». Nature Publishing Group. Nature Education Knowledge. SciTable. 1 (1): 63 
  4. ↑ McCarthy D, Minner C, Bernstein H, Bernstein C (October 1976). «DNA elongation rates and growing point distributions of wild-type phage T4 and a DNA-delay amber mutant». jornal of Molecular Biology. 106 (4): 963–81. PMID 789903. doi:10.1016/0022-2836(76)90346-6  Verifique data em: |data= (ajuda)
  5. ↑ a b Lobo I, Shaw K (2008). «Discovery and Types of Genetic Linkage». Nature Publishing Group. Nature Education Knowledge. SciTable. 1 (1): 139 
  6. ↑ Nachman MW, Crowell SL (September 2000). «Estimate of the mutation rate per nucleotide in humans». Genetics. 156 (1): 297–304. PMC 1461236Acessível livremente. PMID 10978293  Verifique data em: |data= (ajuda)
  7. ↑ Roach JC, Glusman G, Smit AF, Huff CD, Hubley R, Shannon PT, Rowen L, Pant KP, Goodman N, Bamshad M, Shendure J, Drmanac R, Jorde LB, Hood L, Galas DJ (April 2010). «Analysis of genetic inheritance in a family quartet by whole-genome sequencing». Science. 328 (5978): 636–9. Bibcode:2010Sci...328..636R. PMC 3037280Acessível livremente. PMID 20220176. doi:10.1126/science.1186802  Verifique data em: |data= (ajuda)
  8. ↑ a b Drake JW, Charlesworth B, Charlesworth D, Crow JF (April 1998). «Rates of spontaneous mutation». Genetics. 148 (4): 1667–86. PMC 1460098Acessível livremente. PMID 9560386  Verifique data em: |data= (ajuda)
  9. ↑ «What kinds of gene mutations are possible?». Genetics Home Reference. United States National Library of Medicine. 11 May 2015  Parâmetro desconhecido |access-data= ignorado (ajuda); Verifique data em: |data= (ajuda)
  10. ↑ Andrews, Christine A. (2010). «Natural Selection, Genetic Drift, and Gene Flow Do Not Act in Isolation in Natural Populations». Nature Publishing Group. Nature Education Knowledge. SciTable. 3 (10): 5 
  11. ↑ Patterson C (November 1988). «Homology in classical and molecular biology». Molecular Biology and Evolution. 5 (6): 603–25. PMID 3065587. doi:10.1093/oxfordjornals.molbev.a040523  Verifique data em: |data= (ajuda)
  12. ↑ Studer RA, Robinson-Rechavi M (May 2009). «How confident can we be that orthologs are similar, but paralogs differ?». Trends in Genetics. 25 (5): 210–6. PMID 19368988. doi:10.1016/j.tig.2009.03.004  Verifique data em: |data= (ajuda)
  13. ↑ Altenhoff AM, Studer RA, Robinson-Rechavi M, Dessimoz C (2012). «Resolving the ortholog conjecture: orthologs tend to be weakly, but significantly, more similar in function than paralogs». PLOS Computational Biology. 8 (5): e1002514. Bibcode:2012PLSCB...8E2514A. PMC 3355068Acessível livremente. PMID 22615551. doi:10.1371/jornal.pcbi.1002514  publicação de acesso livre - leitura gratuita
  14. ↑ Nosil P, Funk DJ, Ortiz-Barrientos D (February 2009). «Divergent selection and heterogeneous genomic divergence». Molecular Ecology. 18 (3): 375–402. PMID 19143936. doi:10.1111/j.1365-294X.2008.03946.x  Verifique data em: |data= (ajuda)
  15. ↑ Emery, Laura (5 December 2014). «Introduction to Phylogenetics». EMBL-EBI  Parâmetro desconhecido |access-data= ignorado (ajuda); Verifique data em: |data= (ajuda)
  16. ↑ Mitchell MW, Gonder MK (2013). «Primate Speciation: A Case Study of African Apes». Nature Publishing Group. Nature Education Knowledge. SciTable. 4 (2): 1 
  17. ↑ a b Guerzoni D, McLysaght A (November 2011). «De novo origins of human genes». PLOS Genetics. 7 (11): e1002381. PMC 3213182Acessível livremente. PMID 22102832. doi:10.1371/jornal.pgen.1002381  Verifique data em: |data= (ajuda) publicação de acesso livre - leitura gratuita
  18. ↑ Reams AB, Roth JR (February 2015). «Mechanisms of gene duplication and amplification». Cold Spring Harbor Perspectives in Biology. 7 (2): a016592. PMC 4315931Acessível livremente. PMID 25646380. doi:10.1101/cshperspect.a016592  Verifique data em: |data= (ajuda)
  19. ↑ Demuth JP, De Bie T, Stajich JE, Cristianini N, Hahn MW (December 2006). «The evolution of mammalian gene families». PLOS ONE. 1 (1): e85. Bibcode:2006PLoSO...1...85D. PMC 1762380Acessível livremente. PMID 17183716. doi:10.1371/jornal.pone.0000085  Verifique data em: |data= (ajuda) publicação de acesso livre - leitura gratuita
  20. ↑ Knowles DG, McLysaght A (October 2009). «Recent de novo origin of human protein-coding genes». Genome Research. 19 (10): 1752–9. PMC 2765279Acessível livremente. PMID 19726446. doi:10.1101/gr.095026.109  Verifique data em: |data= (ajuda)
  21. ↑ Wu DD, Irwin DM, Zhang YP (November 2011). «De novo origin of human protein-coding genes». PLOS Genetics. 7 (11): e1002379. PMC 3213175Acessível livremente. PMID 22102831. doi:10.1371/jornal.pgen.1002379  Verifique data em: |data= (ajuda) publicação de acesso livre - leitura gratuita
  22. ↑ McLysaght A, Guerzoni D (September 2015). «New genes from non-coding sequence: the role of de novo protein-coding genes in eukaryotic evolutionary innovation». Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences. 370 (1678). 20140332 páginas. PMC 4571571Acessível livremente. PMID 26323763. doi:10.1098/rstb.2014.0332  Verifique data em: |data= (ajuda)
  23. ↑ Neme R, Tautz D (February 2013). «Phylogenetic patterns of emergence of new genes support a model of frequent de novo evolution». BMC Genomics. 14 (1). 117 páginas. PMC 3616865Acessível livremente. PMID 23433480. doi:10.1186/1471-2164-14-117  Verifique data em: |data= (ajuda)
  24. ↑ Treangen TJ, Rocha EP (January 2011). «Horizontal transfer, not duplication, drives the expansion of protein families in prokaryotes». PLOS Genetics. 7 (1): e1001284. PMC 3029252Acessível livremente. PMID 21298028. doi:10.1371/jornal.pgen.1001284  Verifique data em: |data= (ajuda) publicação de acesso livre - leitura gratuita
  25. ↑ Erro de citação: Etiqueta <ref> inválida; não foi fornecido texto para as refs de nome bennett
  26. ↑ Ochman H, Lawrence JG, Groisman EA (May 2000). «Lateral gene transfer and the nature of bacterial innovation». Nature. 405 (6784): 299–304. Bibcode:2000Natur.405..299O. PMID 10830951. doi:10.1038/35012500  Parâmetro desconhecido |= ignorado (ajuda); Verifique data em: |data= (ajuda)
  27. ↑ Keeling PJ, Palmer JD (August 2008). «Horizontal gene transfer in eukaryotic evolution». Nature Reviews Genetics. 9 (8): 605–18. PMID 18591983. doi:10.1038/nrg2386  Parâmetro desconhecido |= ignorado (ajuda); Verifique data em: |data= (ajuda)
  28. ↑ Schönknecht G, Chen WH, Ternes CM, Barbier GG, Shrestha RP, Stanke M, Bräutigam A, Baker BJ, Banfield JF, Garavito RM, Carr K, Wilkerson C, Rensing SA, Gagneul D, Dickenson NE, Oesterhelt C, Lercher MJ, Weber AP (March 2013). «Gene transfer from bacteria and archaea facilitated evolution of an extremophilic eukaryote». Science. 339 (6124): 1207–10. Bibcode:2013Sci...339.1207S. PMID 23471408. doi:10.1126/science.1231707  Parâmetro desconhecido |= ignorado (ajuda); Verifique data em: |data= (ajuda)
  29. ↑ Ridley, M. (2006). Genome. New York, NY: Harper Perennial. ISBN 0-06-019497-9
  30. ↑ Watson, JD, Baker TA, Bell SP, Gann A, Levine M, Losick R. (2004). "Ch9-10", Molecular Biology of the Gene, 5th ed., Peason Benjamin Cummings; CSHL Press.
  31. ↑ «Integr8 – A.thaliana Genome Statistics» 
  32. ↑ «Understanding the Basics». The Human Genome Project  Parâmetro desconhecido |access-data= ignorado (ajuda)
  33. ↑ «WS227 Release Letter». WormBase. 10 August 2011. Cópia arquivada em |arquivourl= requer |arquivodata= (ajuda) 🔗  Parâmetro desconhecido |access-data= ignorado (ajuda); Parâmetro desconhecido |archive-data= ignorado (ajuda); Verifique data em: |data= (ajuda)
  34. ↑ a b Yu J, Hu S, Wang J, Wong GK, Li S, Liu B et al. (April 2002). «A draft sequence of the rice genome (Oryza sativa L. ssp. indica)». Science. 296 (5565): 79–92. Bibcode:2002Sci...296...79Y. PMID 11935017. doi:10.1126/science.1068037  Parâmetro desconhecido |= ignorado (ajuda); Verifique data em: |data= (ajuda)
  35. ↑ a b Anderson S, Bankier AT, Barrell BG, de Bruijn MH, Coulson AR, Drouin J, Eperon IC, Nierlich DP, Roe BA, Sanger F, Schreier PH, Smith AJ, Staden R, Young IG (April 1981). «Sequence and organization of the human mitochondrial genome». Nature. 290 (5806): 457–65. Bibcode:1981Natur.290..457A. PMID 7219534. doi:10.1038/290457a0  Parâmetro desconhecido |= ignorado (ajuda); Verifique data em: |data= (ajuda)
  36. ↑ Adams MD, Celniker SE, Holt RA, Evans CA, Gocayne JD, Amanatides PG et al. (March 2000). «The genome sequence of Drosophila melanogaster». Science. 287 (5461): 2185–95. Bibcode:2000Sci...287.2185.. CiteSeerX 10.1.1.549.8639Acessível livremente. PMID 10731132. doi:10.1126/science.287.5461.2185  Verifique data em: |data= (ajuda)
  37. ↑ a b Pertea M, Salzberg SL (2010). «Between a chicken and a grape: estimating the number of human genes». Genome Biology. 11 (5). 206 páginas. PMC 2898077Acessível livremente. PMID 20441615. doi:10.1186/gb-2010-11-5-206 
  38. ↑ Belyi VA, Levine AJ, Skalka AM (December 2010). «Sequences from ancestral single-stranded DNA viruses in vertebrate genomes: the parvoviridae and circoviridae are more than 40 to 50 million years old». jornal of Virology. 84 (23): 12458–62. PMC 2976387Acessível livremente. PMID 20861255. doi:10.1128/JVI.01789-10  Verifique data em: |data= (ajuda)
  39. ↑ Flores R, Di Serio F, Hernández C (February 1997). «Viroids: The Noncoding Genomes». Seminars in Virology. 8 (1): 65–73. doi:10.1006/smvy.1997.0107  Verifique data em: |data= (ajuda)
  40. ↑ Zonneveld, B.J.M. (2010). «New Record Holders for Maximum Genome Size in Eudicots and Monocots». jornal of Botany. 2010: 1–4. doi:10.1155/2010/527357 
  41. ↑ Perez-Iratxeta C, Palidwor G, Andrade-Navarro MA (December 2007). «Towards completion of the Earth's proteome». EMBO Reports. 8 (12): 1135–41. PMC 2267224Acessível livremente. PMID 18059312. doi:10.1038/sj.embor.7401117  Verifique data em: |data= (ajuda)
  42. ↑ Kauffman SA (March 1969). «Metabolic stability and epigenesis in randomly constructed genetic nets». Elsevier. jornal of Theoretical Biology. 22 (3): 437–67. PMID 5803332. doi:10.1016/0022-5193(69)90015-0  Verifique data em: |data= (ajuda)
  43. ↑ Schuler GD, Boguski MS, Stewart EA, Stein LD, Gyapay G, Rice K et al. (October 1996). «A gene map of the human genome». Science. 274 (5287): 540–6. Bibcode:1996Sci...274..540S. PMID 8849440. doi:10.1126/science.274.5287.540  Parâmetro desconhecido |= ignorado (ajuda); Verifique data em: |data= (ajuda)
  44. ↑ Chi KR (October 2016). «The dark side of the human genome». Nature (em inglês). 538 (7624): 275–277. Bibcode:2016Natur.538..275C. PMID 27734873. doi:10.1038/538275a  Verifique data em: |data= (ajuda)
  45. ↑ a b Claverie JM (September 2005). «Fewer genes, more noncoding RNA». Science. 309 (5740): 1529–30. Bibcode:2005Sci...309.1529C. PMID 16141064. doi:10.1126/science.1116800  Parâmetro desconhecido |= ignorado (ajuda); Verifique data em: |data= (ajuda)
  46. ↑ Carninci P, Hayashizaki Y (April 2007). «Noncoding RNA transcription beyond annotated genes». Current Opinion in Genetics & Development. 17 (2): 139–44. PMID 17317145. doi:10.1016/j.gde.2007.02.008  Verifique data em: |data= (ajuda)
  47. ↑ a b Hutchison CA, Chuang RY, Noskov VN, Assad-Garcia N, Deerinck TJ, Ellisman MH, Gill J, Kannan K, Karas BJ, Ma L, Pelletier JF, Qi ZQ, Richter RA, Strychalski EA, Sun L, Suzuki Y, Tsvetanova B, Wise KS, Smith HO, Glass JI, Merryman C, Gibson DG, Venter JC (March 2016). «Design and synthesis of a minimal bacterial genome». Science. 351 (6280): aad6253. Bibcode:2016Sci...351.....H. PMID 27013737. doi:10.1126/science.aad6253  Verifique data em: |data= (ajuda)
  48. ↑ Glass JI, Assad-Garcia N, Alperovich N, Yooseph S, Lewis MR, Maruf M, Hutchison CA, Smith HO, Venter JC (January 2006). «Essential genes of a minimal bacterium». Proceedings of the National Academy of Sciences of the United States of America. 103 (2): 425–30. Bibcode:2006PNAS..103..425G. PMC 1324956Acessível livremente. PMID 16407165. doi:10.1073/pnas.0510013103  Verifique data em: |data= (ajuda)
  49. ↑ Gerdes SY, Scholle MD, Campbell JW, Balázsi G, Ravasz E, Daugherty MD, Somera AL, Kyrpides NC, Anderson I, Gelfand MS, Bhattacharya A, Kapatral V, D'Souza M, Baev MV, Grechkin Y, Mseeh F, Fonstein MY, Overbeek R, Barabási AL, Oltvai ZN, Osterman AL (October 2003). «Experimental determination and system level analysis of essential genes in Escherichia coli MG1655». jornal of Bacteriology. 185 (19): 5673–84. PMC 193955Acessível livremente. PMID 13129938. doi:10.1128/jb.185.19.5673-5684.2003  Verifique data em: |data= (ajuda)
  50. ↑ Baba T, Ara T, Hasegawa M, Takai Y, Okumura Y, Baba M, Datsenko KA, Tomita M, Wanner BL, Mori H (2006). «Construction of Escherichia coli K-12 in-frame, single-gene knockout mutants: the Keio collection». Molecular Systems Biology. 2. 2006.0008 páginas. PMC 1681482Acessível livremente. PMID 16738554. doi:10.1038/msb4100050 
  51. ↑ a b Juhas M, Reuß DR, Zhu B, Commichau FM (November 2014). «Bacillus subtilis and Escherichia coli essential genes and minimal cell factories after one decade of genome engineering». Microbiology. 160 (Pt 11): 2341–2351. PMID 25092907. doi:10.1099/mic.0.079376-0  Verifique data em: |data= (ajuda)
  52. ↑ Tu Z, Wang L, Xu M, Zhou X, Chen T, Sun F (February 2006). «Further understanding human disease genes by comparing with housekeeping genes and other genes». BMC Genomics. 7. 31 páginas. PMC 1397819Acessível livremente. PMID 16504025. doi:10.1186/1471-2164-7-31  Verifique data em: |data= (ajuda) publicação de acesso livre - leitura gratuita
  53. ↑ Georgi B, Voight BF, Bućan M (May 2013). «From mouse to human: evolutionary genomics analysis of human orthologs of essential genes». PLOS Genetics. 9 (5): e1003484. PMC 3649967Acessível livremente. PMID 23675308. doi:10.1371/jornal.pgen.1003484  Verifique data em: |data= (ajuda) publicação de acesso livre - leitura gratuita
  54. ↑ Eisenberg E, Levanon EY (October 2013). «Human housekeeping genes, revisited». Trends in Genetics. 29 (10): 569–74. PMID 23810203. doi:10.1016/j.tig.2013.05.010  Verifique data em: |data= (ajuda)
  55. ↑ Amsterdam A, Hopkins N (September 2006). «Mutagenesis strategies in zebrafish for identifying genes involved in development and disease». Trends in Genetics. 22 (9): 473–8. PMID 16844256. doi:10.1016/j.tig.2006.06.011  Verifique data em: |data= (ajuda)
  56. ↑ «About the HGNC». HGNC Database of Human Gene Names. HUGO Gene Nomenclature Committee  Parâmetro desconhecido |access-data= ignorado (ajuda)
  57. ↑ Cohen SN, Chang AC (May 1973). «Recircularization and autonomous replication of a sheared R-factor DNA segment in Escherichia coli transformants». Proceedings of the National Academy of Sciences of the United States of America. 70 (5): 1293–7. Bibcode:1973PNAS...70.1293C. PMC 433482Acessível livremente. PMID 4576014. doi:10.1073/pnas.70.5.1293  Verifique data em: |data= (ajuda)
  58. ↑ Esvelt KM, Wang HH (2013). «Genome-scale engineering for systems and synthetic biology». Molecular Systems Biology. 9 (1). 641 páginas. PMC 3564264Acessível livremente. PMID 23340847. doi:10.1038/msb.2012.66 
  59. ↑ Tan WS, Carlson DF, Walton MW, Fahrenkrug SC, Hackett PB (2012). «Precision editing of large animal genomes». Advances in Genetics Volume 80. Col: Advances in Genetics. 80. [S.l.: s.n.] pp. 37–97. ISBN 9780124047426. PMC 3683964Acessível livremente. PMID 23084873. doi:10.1016/B978-0-12-404742-6.00002-8 
  60. ↑ Puchta H, Fauser F (2013). «Gene targeting in plants: 25 years later». The International jornal of Developmental Biology. 57 (6–8): 629–37. PMID 24166445. doi:10.1387/ijdb.130194hp 
  61. ↑ Ran FA, Hsu PD, Wright J, Agarwala V, Scott DA, Zhang F (November 2013). «Genome engineering using the CRISPR-Cas9 system». Nature Protocols. 8 (11): 2281–2308. PMC 3969860Acessível livremente. PMID 24157548. doi:10.1038/nprot.2013.143  Verifique data em: |data= (ajuda)
  62. ↑ Kittleson JT, Wu GC, Anderson JC (August 2012). «Successes and failures in modular genetic engineering». Current Opinion in Chemical Biology. 16 (3–4): 329–36. PMID 22818777. doi:10.1016/j.cbpa.2012.06.009  Verifique data em: |data= (ajuda)
  63. ↑ Berg P, Mertz JE (January 2010). «Personal reflections on the origins and emergence of recombinant DNA technology». Genetics. 184 (1): 9–17. PMC 2815933Acessível livremente. PMID 20061565. doi:10.1534/genetics.109.112144  Verifique data em: |data= (ajuda)
  64. ↑ Austin CP, Battey JF, Bradley A, Bucan M, Capecchi M, Collins FS, Dove WF, Duyk G, Dymecki S, Eppig JT, Grieder FB, Heintz N, Hicks G, Insel TR, Joyner A, Koller BH, Lloyd KC, Magnuson T, Moore MW, Nagy A, Pollock JD, Roses AD, Sands AT, Seed B, Skarnes WC, Snoddy J, Soriano P, Stewart DJ, Stewart F, Stillman B, Varmus H, Varticovski L, Verma IM, Vogt TF, von Melchner H, Witkowski J, Woychik RP, Wurst W, Yancopoulos GD, Young SG, Zambrowicz B (September 2004). «The knockout mouse project». Nature Genetics. 36 (9): 921–4. PMC 2716027Acessível livremente. PMID 15340423. doi:10.1038/ng0904-921  Verifique data em: |data= (ajuda)
  65. ↑ Guan C, Ye C, Yang X, Gao J (February 2010). «A review of current large-scale mouse knockout efforts». Genesis. 48 (2): 73–85. PMID 20095055. doi:10.1002/dvg.20594  Verifique data em: |data= (ajuda)
  66. ↑ Deng C (October 2007). «In celebration of Dr. Mario R. Capecchi's Nobel Prize». International jornal of Biological Sciences. 3 (7): 417–9. PMC 2043165Acessível livremente. PMID 17998949. doi:10.7150/ijbs.3.417  Verifique data em: |data= (ajuda)
Obtida de "https://pt.wikipedia.org/w/index.php?title=Usuária:Pwoli/Testes/Gene&oldid=59579828"