This is a good article. Click here for more information.


From Wikipedia, the free encyclopedia
Jump to: navigation, search
This article is about the heritable unit for transmission of biological traits. For other uses, see Gene (disambiguation).
The image above contains clickable links

A gene is a locus (or region) of DNA which is made up of nucleotides and is the molecular unit of heredity.[1][2]:Glossary The transmission of genes to an organism's offspring is the basis of the inheritance of phenotypic traits. Most biological traits are under the influence of polygenes (many different genes) as well as the gene–environment interactions. Some genetic traits are instantly visible, such as eye colour or number of limbs, and some are not, such as blood type, risk for specific diseases, or the thousands of basic biochemical processes that comprise life.

Genes can acquire mutations in their sequence, leading to different variants, known as alleles, in the population. These alleles encode slightly different versions of a protein, which cause different phenotype traits. Colloquial usage of the term "having a gene" (e.g., "good genes," "hair colour gene") typically refers to having a different allele of the gene. Genes evolve due to natural selection or survival of the fittest of the alleles.



Photograph of Gregor Mendel
Gregor Mendel
Main article: History of genetics

Discovery of discrete inherited units[edit]

The existence of discrete inheritable units was first suggested by Gregor Mendel (1822–1884).[6] From 1857 to 1864, he studied inheritance patterns in 8000 common edible pea plants, tracking distinct traits from parent to offspring. He described these mathematically as 2n combinations where n is the number of differing characteristics in the original peas. Although he did not use the term gene, he explained his results in terms of discrete inherited units that give rise to observable physical characteristics. This description prefigured the distinction between genotype (the genetic material of an organism) and phenotype (the visible traits of that organism). Mendel was also the first to demonstrate independent assortment, the distinction between dominant and recessive traits, the distinction between a heterozygote and homozygote, and the phenomenon of discontinuous inheritance.



Sixteen years later, in 1905, the word genetics was first used by William Bateson,[11] while Eduard Strasburger, amongst others, still used the term pangene for the fundamental physical and functional unit of heredity.[12] In 1909 the Danish botanist Wilhelm Johannsen shortened the name to "gene".[13]

Discovery of DNA[edit]

Advances in understanding genes and inheritance continued throughout the 20th century. Deoxyribonucleic acid (DNA) was shown to be the molecular repository of genetic information by experiments in the 1940s to 1950s.[14][15] The structure of DNA was studied by Rosalind Franklin and Maurice Wilkins using X-ray crystallography, which led James D. Watson and Francis Crick to publish a model of the double-stranded DNA molecule whose paired nucleotide bases indicated a compelling hypothesis for the mechanism of genetic replication.[16][17] Collectively, this body of research established the central dogma of molecular biology, which states that proteins are translated from RNA, which is transcribed from DNA. This dogma has since been shown to have exceptions, such as reverse transcription in retroviruses. The modern study of genetics at the level of DNA is known as molecular genetics.


Modern evolutionary synthesis[edit]

The theories developed in the 1930s and 1940s to integrate molecular genetics with Darwinian evolution are called the modern evolutionary synthesis, a term introduced by Julian Huxley.[21] Evolutionary biologists subsequently refined this concept, such as George C. Williams' gene-centric view of evolution. He proposed an evolutionary concept of the gene as a unit of natural selection with the definition: "that which segregates and recombines with appreciable frequency."[22]:24 In this view, the molecular gene transcribes as a unit, and the evolutionary gene inherits as a unit. Related ideas emphasizing the centrality of genes in evolution were popularized by Richard Dawkins.[23][24]

Molecular basis[edit]

Main article: DNA







A microscopy image of 46 chromosomes striped with red and green bands


The majority of eukaryotic genes are stored on a set of large, linear chromosomes. The chromosomes are packed within the nucleus in complex with storage proteins called histones to form a unit called a nucleosome. DNA packaged and condensed in this way is called chromatin.[2]:4.2 The manner in which DNA is stored on the histones, as well as chemical modifications of the histone itself, regulate whether a particular region of DNA is accessible for gene expression. In addition to genes, eukaryotic chromosomes contain sequences involved in ensuring that the DNA is copied without degradation of end regions and sorted into daughter cells during cell division: replication origins, telomeres and the centromere.[2]:4.2 Replication origins are the sequence regions where DNA replication is initiated to make two copies of the chromosome. Telomeres are long stretches of repetitive sequence that cap the ends of the linear chromosomes and prevent degradation of coding and regulatory regions during DNA replication. The length of the telomeres decreases each time the genome is replicated and has been implicated in the aging process.[27] The centromere is required for binding spindle fibres to separate sister chromatids into daughter cells during cell division.[2]:18.2



Structure and function[edit]

The image above contains clickable links
The structure of a eukaryotic protein-coding gene. Regulatory sequence controls when and where expression occurs for the protein coding region (red). Promoter and enhancer regions (yellow) regulate the transcription of the gene into a pre-mRNA which is modified to add a 5' cap and poly-A tail (grey) and remove introns. The mRNA 5' and 3' untranslated regions (blue) regulate translation into the final protein product.
The image above contains clickable links
The structure of a prokaryotic operon of protein-coding genes. Regulatory sequence controls when expression occurs for the multiple protein coding regions (red). Promoter, operator and enhancer regions (yellow) regulate the transcription of the gene into an mRNA. The mRNA untranslated regions (blue) regulate translation into the final protein products.


Firstly, flanking the open reading frame, all genes contain a regulatory sequence that is required for their expression. In order to be expressed, genes require a promoter sequence. The promoter is recognized and bound by transcription factors and RNA polymerase to initiate transcription.[2]:7.1 A gene can have more than one promoter, resulting in messenger RNAs (mRNA) that differ in how far they extend in the 5' end.[30] Promoter regions have a consensus sequence, however highly transcribed genes have "strong" promoter sequences that bind the transcription machinery well, whereas others have "weak" promoters that bind poorly and initiate transcription less frequently.[2]:7.2 Eukaryotic promoter regions are much more complex and difficult to identify than prokaryotic promoters.[2]:7.3

Additionally, genes can have regulatory regions many kilobases upstream or downstream of the open reading frame. These act by binding to transcription factors which then cause the DNA to loop so that the regulatory sequence (and bound transcription factor) become close to the RNA polymerase binding site.[31] For example, enhancers increase transcription by binding an activator protein which then helps to recruit the RNA polymerase to the promoter; conversely silencers bind repressor proteins and make the DNA less available for RNA polymerase.[32]

The transcribed pre-mRNA contains untranslated regions at both ends which contain a ribosome binding site, terminator and start and stop codons.[33] In addition, most eukaryotic open reading frames contain untranslated introns which are removed before the exons are translated. The sequences at the ends of the introns, dictate the splice sites to generate the final mature mRNA which encodes the protein or RNA product.[34]

Many prokaryotic genes are organized into operons, with multiple protein-coding sequences that are transcribed as a unit.[35][36] The products of operon genes typically have related functions and are involved in the same regulatory network.[2]:7.3

Functional definitions[edit]


Early work in molecular genetics suggested the model that one gene makes one protein. This model has been refined since the discovery of genes that can encode multiple proteins by alternative splicing and coding sequences split in short section across the genome whose mRNAs are concatenated by trans-splicing.[5][39][40]


Gene expression[edit]

Main article: Gene expression

In all organisms, two steps are required to read the information encoded in a gene's DNA and produce the protein it specifies. First, the gene's DNA is transcribed to messenger RNA (mRNA).[2]:6.1 Second, that mRNA is translated to protein.[2]:6.2 RNA-coding genes must still go through the first step, but are not translated into protein.[41] The process of producing a biologically functional molecule of either RNA or protein is called gene expression, and the resulting molecule is called a gene product.

Genetic code[edit]











RNA genes[edit]


Some viruses store their entire genomes in the form of RNA, and contain no DNA at all.[45][46] Because they use RNA to store genes, their cellular hosts may synthesize their proteins as soon as they are infected and without the delay in waiting for transcription.[47] On the other hand, RNA retroviruses, such as HIV, require the reverse transcription of their genome from RNA into DNA before their proteins can be synthesized. RNA-mediated epigenetic inheritance has also been observed in plants and very rarely in animals.[48]


Inheritance of a gene that has two different alleles (blue and white). The gene is located on an autosomal chromosome. The blue allele is recessive to the white allele. The probability of each outcome in the children's generation is one quarter, or 25 percent.
Main articles: Mendelian inheritance and Heredity


Mendelian inheritance[edit]

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 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.[2]:20


DNA replication and cell division[edit]



Molecular inheritance[edit]



Molecular evolution[edit]

Main article: Molecular evolution


DNA replication is for the most part extremely accurate, however errors (mutations) do occur.[2]:7.6 The error rate in eukaryotic cells can be as low as 10−8 per nucleotide per replication,[52][53] whereas for some RNA viruses it can be as high as 10−3.[54] This means that each generation, each human genome accumulates 1–2 new mutations.[54] 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).[55] 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, the DNA repair mechanisms that normally revert mutations can introduce errors when repairing the physical damage to the molecule is more important than restoring an exact copy, for example when repairing double-strand breaks.[2]:5.4



Sequence homology[edit]

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.[57] 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,[2]: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.[58][59]

The relationship between genes can be measured by comparing the sequence alignment of their DNA.[2]: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.[60] 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.[61][62]

Origins of new genes[edit]

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.[63][64] The resulting genes (paralogs) may then diverge in sequence and in function. Sets of genes formed in this way comprise a gene family. Gene duplications and losses within a family are common and represent a major source of evolutionary biodiversity.[65] 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.[2]:7.6

De novo or "orphan" genes, whose sequence shows no similarity to existing genes, are extremely rare. Estimates of the number of de novo genes in the human genome range from 18[66] to 60.[67] Such genes are typically shorter and simpler in structure than most eukaryotic genes, with few if any introns.[63] Two primary sources of orphan protein-coding genes are gene duplication followed by extremely rapid sequence change, such that the original relationship is undetectable by sequence comparisons, and formation through mutation of "cryptic" transcription start sites that introduce a new open reading frame in a region of the genome that did not previously code for a protein.[68][69]

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.[70] It is a common means of spreading antibiotic resistance, virulence, and adaptive metabolic functions.[28][71] Although horizontal gene transfer is rare in eukaryotes, likely examples have been identified of protist and alga genomes containing genes of bacterial origin.[72][73]



Number of genes[edit]


The genome size, and the number of genes it encodes varies widely between organisms. The smallest genomes occur in viruses (which can have as few as 2 protein-coding genes),[83] and viroids (which act as a single non-coding RNA gene).[84] Conversely, plants can have extremely large genomes,[85] with rice containing >46,000 protein-coding genes.[86] The total number of protein-coding genes (the Earth's proteome) is estimated to be 5 million sequences.[87]

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.[88] Early experimental measures indicated there to be 50,000–100,000 transcribed genes (expressed sequence tags).[89] 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[82] with 13 genes encoded on the mitochondrial genome.[80] Of the human genome, only 1–2% consists of protein-coding genes,[90] with the remainder being 'noncoding' DNA such as introns, retrotransposons, and noncoding RNAs.[90][91]Every organism has all his genes in all cells of his body but it is not important that every gene must function in every cell .

Essential genes[edit]

Main article: Essential gene
Gene functions in the minimal genome of the synthetic organism, Syn 3.[92]

Essential genes are the set of genes thought to be critical for an organism's survival.[93] 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.[94][95][96] Half of these genes are orthologs in both organisms and are largely involved in protein synthesis.[96] In the budding yeast Saccharomyces cerevisiae the number of essential genes is slightly higher, at 1000 genes (~20% of their genes).[97] 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).[98] 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.[92]

Essential genes include Housekeeping genes (critical for basic cell functions)[99] as well as genes that are expressed at different times in the organisms development or life cycle.[100] 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[edit]


Genetic engineering[edit]

Comparison of conventional plant breeding with transgenic and cisgenic genetic modification.
Main article: 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.[102] 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.[103][104][105][106] The related term synthetic biology is sometimes used to refer to extensive genetic engineering of an organism.[107]

Genetic engineering is now a routine research tool with model organisms. For example, genes are easily added to bacteria[108] and lineages of knockout mice with a specific gene's function disrupted are used to investigate that gene's function.[109][110] 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.[111] However, the genomes of cells in an adult organism can be edited using gene therapy techniques to treat genetic diseases.

See also[edit]


Main textbook[edit]

Alberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P (2002). Molecular Biology of the Cell (Fourth ed.). New York: Garland Science. ISBN 978-0-8153-3218-3.  – A molecular biology textbook available free online through NCBI access publication - free to read


  1. ^ Slack, J.M.W. Genes-A Very Short Introduction. Oxford University Press 2014
  3. ^ a b Gericke, Niklas Markus; Hagberg, Mariana (5 December 2006). "Definition of historical models of gene function and their relation to students' understanding of genetics". Science & Education 16 (7–8): 849–881. Bibcode:2007Sc&Ed..16..849G. doi:10.1007/s11191-006-9064-4. 
  5. ^ a b c Pennisi E (June 2007). "Genomics. DNA study forces rethink of what it means to be a gene". Science 316 (5831): 1556–1557. doi:10.1126/science.316.5831.1556. PMID 17569836. 
  6. ^ Noble D (September 2008). "Genes and causation" (Free full text). Philosophical Transactions. Series A, Mathematical, Physical, and Engineering Sciences 366 (1878): 3001–3015. Bibcode:2008RSPTA.366.3001N. doi:10.1098/rsta.2008.0086. PMID 18559318. 
  12. ^ Gager, C.S., Translator's preface to Intracellular Pangenesis, page viii.
  13. ^ "The Human Genome Project Timeline". Retrieved 13 September 2006. 
  15. ^ Hershey, AD; Chase, M (1952). "Independent functions of viral protein and nucleic acid in growth of bacteriophage". The Journal of General Physiology 36 (1): 39–56. doi:10.1085/jgp.36.1.39. PMC 2147348. PMID 12981234. 
  17. ^ Watson, J. D.; Crick, FH (1953). "Molecular Structure of Nucleic Acids: A Structure for Deoxyribose Nucleic Acid" (PDF). Nature 171 (4356): 737–8. Bibcode:1953Natur.171..737W. doi:10.1038/171737a0. PMID 13054692. 
  20. ^ Adams, Jill U. (2008). "DNA Sequencing Technologies". Nature Education Knowledge. SciTable (Nature Publishing Group) 1 (1): 193. 
  21. ^ Huxley, Julian (1942). Evolution: the modern synthesis (Definitive ed.). Cambridge, Mass.: MIT Press. ISBN 978-0262513661. 
  22. ^ Williams, George C. (2001). Adaptation and Natural Selection a Critique of Some Current Evolutionary Thought. ([Online-Ausg.]. ed.). Princeton: Princeton University Press. ISBN 9781400820108. 
  23. ^ Dawkins, Richard (1977). The selfish gene (Repr. (with corr.) ed.). London: Oxford Univ. Press. ISBN 0-19-857519-X. 
  24. ^ Dawkins, Richard (1989). The extended phenotype. (Pbk. ed.). Oxford: Oxford University Press. ISBN 0-19-286088-7. 
  26. ^ Bolzer, Andreas; Kreth, Gregor; Solovei, Irina; Koehler, Daniela; Saracoglu, Kaan; Fauth, Christine; Müller, Stefan; Eils, Roland; Cremer, Christoph; Speicher, Michael R.; Cremer, Thomas (2005). "Three-Dimensional Maps of All Chromosomes in Human Male Fibroblast Nuclei and Prometaphase Rosettes". PLoS Biology 3 (5): e157. doi:10.1371/journal.pbio.0030157. PMID 15839726.  open access publication - free to read
  27. ^ Braig M, Schmitt CA (March 2006). "Oncogene-induced senescence: putting the brakes on tumor development". Cancer Research 66 (6): 2881–4. doi:10.1158/0008-5472.CAN-05-4006. PMID 16540631. 
  28. ^ a b Bennett, PM (March 2008). "Plasmid encoded antibiotic resistance: acquisition and transfer of antibiotic resistance genes in bacteria.". British Journal of Pharmacology. 153 Suppl 1: S347–57. doi:10.1038/sj.bjp.0707607. PMC 2268074. PMID 18193080. 
  30. ^ Mortazavi A, Williams BA, McCue K, Schaeffer L, Wold B (July 2008). "Mapping and quantifying mammalian transcriptomes by RNA-Seq". Nature Methods 5 (7): 621–8. doi:10.1038/nmeth.1226. PMID 18516045. 
  31. ^ Pennacchio, L. A.; Bickmore, W.; Dean, A.; Nobrega, M. A.; Bejerano, G. (2013). "Enhancers: Five essential questions". Nature Reviews Genetics 14 (4): 288–95. doi:10.1038/nrg3458. PMID 23503198. 
  32. ^ Maston, G. A.; Evans, S. K.; Green, M. R. (2006). "Transcriptional Regulatory Elements in the Human Genome". Annual Review of Genomics and Human Genetics 7: 29–59. doi:10.1146/annurev.genom.7.080505.115623. PMID 16719718. 
  33. ^ Mignone, Flavio; Gissi, Carmela; Liuni, Sabino; Pesole, Graziano (2002-02-28). "Untranslated regions of mRNAs". Genome Biology 3 (3): reviews0004. doi:10.1186/gb-2002-3-3-reviews0004. ISSN 1465-6906. PMID 11897027. 
  34. ^ Bicknell AA, Cenik C, Chua HN, Roth FP, Moore MJ (December 2012). "Introns in UTRs: why we should stop ignoring them.". BioEssays 34 (12): 1025–34. doi:10.1002/bies.201200073. PMID 23108796. 
  36. ^ Blumenthal, Thomas (November 2004). "Operons in eukaryotes". Briefings in Functional Genomics & Proteomics 3 (3): 199–211. doi:10.1093/bfgp/3.3.199. ISSN 2041-2649. PMID 15642184. 
  38. ^ Williams, A; Spilianakis, CG; Flavell, RA (April 2010). "Interchromosomal association and gene regulation in trans.". Trends in genetics : TIG 26 (4): 188–97. doi:10.1016/j.tig.2010.01.007. PMID 20236724. 
  40. ^ Parra G, Reymond A, Dabbouseh N, Dermitzakis ET, Castelo R, Thomson TM, Antonarakis SE, Guigó R (January 2006). "Tandem chimerism as a means to increase protein complexity in the human genome". Genome Research 16 (1): 37–44. doi:10.1101/gr.4145906. PMC 1356127. PMID 16344564. 
  42. ^ Crick, Francis (1962). The genetic code. WH Freeman and Company. PMID 13882204. 
  43. ^ Woodson SA (May 1998). "Ironing out the kinks: splicing and translation in bacteria". Genes & Development 12 (9): 1243–7. doi:10.1101/gad.12.9.1243. PMID 9573040. 
  45. ^ Koonin, Eugene V.; Dolja, Valerian V.; Morris, T. Jack (January 1993). "Evolution and Taxonomy of Positive-Strand RNA Viruses: Implications of Comparative Analysis of Amino Acid Sequences". Critical Reviews in Biochemistry and Molecular Biology 28 (5): 375–430. doi:10.3109/10409239309078440. PMID 8269709. 
  46. ^ Domingo, Esteban (2001). "RNA Virus Genomes". ELS. doi:10.1002/9780470015902.a0001488.pub2. ISBN 0470016175. 
  47. ^ Domingo, E; Escarmís, C; Sevilla, N; Moya, A; Elena, SF; Quer, J; Novella, IS; Holland, JJ (June 1996). "Basic concepts in RNA virus evolution.". FASEB Journal 10 (8): 859–64. PMID 8666162. 
  48. ^ Morris, KV; Mattick, JS (June 2014). "The rise of regulatory RNA.". Nature Reviews Genetics 15 (6): 423–37. doi:10.1038/nrg3722. PMID 24776770. 
  49. ^ Miko, Ilona (2008). "Gregor Mendel and the Principles of Inheritance". Nature Education Knowledge. SciTable (Nature Publishing Group) 1 (1): 134. 
  50. ^ Chial, Heidi (2008). "Mendelian Genetics: Patterns of Inheritance and Single-Gene Disorders". Nature Education Knowledge. SciTable (Nature Publishing Group) 1 (1): 63. 
  51. ^ Lobo, Ingrid; Shaw, Kelly (2008). "Discovery and Types of Genetic Linkage". Nature Education Knowledge. SciTable (Nature Publishing Group) 1 (1): 139. 
  52. ^ Nachman MW, Crowell SL (September 2000). "Estimate of the mutation rate per nucleotide in humans". Genetics 156 (1): 297–304. PMC 1461236. PMID 10978293. 
  54. ^ a b Drake JW, Charlesworth B, Charlesworth D, Crow JF (April 1998). "Rates of spontaneous mutation". Genetics 148 (4): 1667–86. PMC 1460098. PMID 9560386. 
  56. ^ Andrews, Christine A. (2010). "Natural Selection, Genetic Drift, and Gene Flow Do Not Act in Isolation in Natural Populations". Nature Education Knowledge. SciTable (Nature Publishing Group) 3 (10): 5. 
  57. ^ Patterson, C (November 1988). "Homology in classical and molecular biology.". Molecular Biology and Evolution 5 (6): 603–25. PMID 3065587. 
  58. ^ Studer, RA; Robinson-Rechavi, M (May 2009). "How confident can we be that orthologs are similar, but paralogs differ?". Trends in genetics : TIG 25 (5): 210–6. doi:10.1016/j.tig.2009.03.004. PMID 19368988. 
  59. ^ 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. doi:10.1371/journal.pcbi.1002514. PMID 22615551.  open access publication - free to read
  60. ^ NOSIL, PATRIK; FUNK, DANIEL J.; ORTIZ-BARRIENTOS, DANIEL (February 2009). "Divergent selection and heterogeneous genomic divergence". Molecular Ecology 18 (3): 375–402. doi:10.1111/j.1365-294X.2008.03946.x. PMID 19143936. 
  62. ^ Mitchell, Matthew W.; Gonder, Mary Katherine (2013). "Primate Speciation: A Case Study of African Apes". Nature Education Knowledge. SciTable (Nature Publishing Group) 4 (2): 1. 
  63. ^ a b Guerzoni, D; McLysaght, A (November 2011). "De novo origins of human genes.". PLOS Genetics 7 (11): e1002381. doi:10.1371/journal.pgen.1002381. PMID 22102832.  open access publication - free to read
  64. ^ Reams, AB; Roth, JR (2 February 2015). "Mechanisms of gene duplication and amplification.". Cold Spring Harbor perspectives in biology 7 (2): a016592. doi:10.1101/cshperspect.a016592. PMID 25646380. 
  65. ^ Demuth, JP; De Bie, T; Stajich, JE; Cristianini, N; Hahn, MW (20 December 2006). "The evolution of mammalian gene families". PLoS ONE 1: e85. Bibcode:2006PLoSO...1...85D. doi:10.1371/journal.pone.0000085. PMC 1762380. PMID 17183716.  open access publication - free to read
  66. ^ Knowles, DG; McLysaght, A (October 2009). "Recent de novo origin of human protein-coding genes.". Genome Research 19 (10): 1752–9. doi:10.1101/gr.095026.109. PMC 2765279. PMID 19726446. 
  67. ^ Wu, DD; Irwin, DM; Zhang, YP (November 2011). "De novo origin of human protein-coding genes.". PLOS Genetics 7 (11): e1002379. doi:10.1371/journal.pgen.1002379. PMC 3213175. PMID 22102831.  open access publication - free to read
  68. ^ Tautz, D; Domazet-Lošo, T (31 August 2011). "The evolutionary origin of orphan genes.". Nature Reviews Genetics 12 (10): 692–702. doi:10.1038/nrg3053. PMID 21878963. 
  69. ^ Carvunis, AR; Rolland, T; Wapinski, I; Calderwood, MA; Yildirim, MA; Simonis, N; Charloteaux, B; Hidalgo, CA; Barbette, J; Santhanam, B; Brar, GA; Weissman, JS; Regev, A; Thierry-Mieg, N; Cusick, ME; Vidal, M (19 July 2012). "Proto-genes and de novo gene birth.". Nature 487 (7407): 370–4. Bibcode:2012Natur.487..370C. doi:10.1038/nature11184. PMID 22722833. 
  70. ^ Treangen, TJ; Rocha, EP (27 January 2011). "Horizontal transfer, not duplication, drives the expansion of protein families in prokaryotes.". PLOS Genetics 7 (1): e1001284. doi:10.1371/journal.pgen.1001284. PMID 21298028.  open access publication - free to read
  71. ^ Ochman, H; Lawrence, JG; Groisman, EA (18 May 2000). "Lateral gene transfer and the nature of bacterial innovation.". Nature 405 (6784): 299–304. Bibcode:2000Natur.405..299O. doi:10.1038/35012500. PMID 10830951. 
  72. ^ Keeling, PJ; Palmer, JD (August 2008). "Horizontal gene transfer in eukaryotic evolution.". Nature Reviews Genetics 9 (8): 605–18. doi:10.1038/nrg2386. PMID 18591983. 
  76. ^ "Integr8 – A.thaliana Genome Statistics:". 
  80. ^ a b Anderson, S.; Bankier, A. T.; Barrell, B. G.; de Bruijn, M. H. L.; Coulson, A. R.; Drouin, J.; Eperon, I. C.; Nierlich, D. P.; Roe, B. A.; Sanger, F.; Schreier, P. H.; Smith, A. J. H.; Staden, R.; Young, I. G. (9 April 1981). "Sequence and organization of the human mitochondrial genome". Nature 290 (5806): 457–465. Bibcode:1981Natur.290..457A. doi:10.1038/290457a0. PMID 7219534. 
  81. ^ Adams, M. D. (24 March 2000). "The Genome Sequence of Drosophila melanogaster". Science 287 (5461): 2185–2195. Bibcode:2000Sci...287.2185.. doi:10.1126/science.287.5461.2185. PMID 10731132. 
  82. ^ a b Pertea, Mihaela; Salzberg, Steven L (2010). "Between a chicken and a grape: estimating the number of human genes". Genome Biology 11 (5): 206. doi:10.1186/gb-2010-11-5-206. PMC 2898077. PMID 20441615. 
  83. ^ Belyi, V. A.; Levine, A. J.; Skalka, A. M. (22 September 2010). "Sequences from Ancestral Single-Stranded DNA Viruses in Vertebrate Genomes: the Parvoviridae and Circoviridae Are More than 40 to 50 Million Years Old". Journal of Virology 84 (23): 12458–12462. doi:10.1128/JVI.01789-10. PMC 2976387. PMID 20861255. 
  84. ^ Flores, Ricardo; Di Serio, Francesco; Hernández, Carmen (February 1997). "Viroids: The Noncoding Genomes". Seminars in Virology 8 (1): 65–73. doi:10.1006/smvy.1997.0107. 
  85. ^ Zonneveld, B. J. M. (2010). "New Record Holders for Maximum Genome Size in Eudicots and Monocots". Journal of Botany 2010: 1–4. doi:10.1155/2010/527357. 
  87. ^ Perez-Iratxeta C, Palidwor G, Andrade-Navarro MA (December 2007). "Towards completion of the Earth's proteome". EMBO Reports 8 (12): 1135–1141. doi:10.1038/sj.embor.7401117. PMC 2267224. PMID 18059312. 
  88. ^ Kauffman SA (1969). "Metabolic stability and epigenesis in randomly constructed genetic nets". Journal of Theoretical Biology (Elsevier) 22 (3): 437–467. doi:10.1016/0022-5193(69)90015-0. PMID 5803332. 
  91. ^ Carninci P, Hayashizaki Y (April 2007). "Noncoding RNA transcription beyond annotated genes". Current Opinion in Genetics & Development 17 (2): 139–44. doi:10.1016/j.gde.2007.02.008. PMID 17317145. 
  92. ^ a b Hutchison, Clyde A.; Chuang, Ray-Yuan; Noskov, Vladimir N.; Assad-Garcia, Nacyra; Deerinck, Thomas J.; Ellisman, Mark H.; Gill, John; Kannan, Krishna; Karas, Bogumil J. (2016-03-25). "Design and synthesis of a minimal bacterial genome". Science 351 (6280): aad6253. Bibcode:2016Sci...351.....H. doi:10.1126/science.aad6253. ISSN 0036-8075. PMID 27013737. 
  93. ^ Glass, J. I.; Assad-Garcia, N.; Alperovich, N.; Yooseph, S.; Lewis, M. R.; Maruf, M.; Hutchison, C. A.; Smith, H. O.; Venter, J. C. (3 January 2006). "Essential genes of a minimal bacterium". Proceedings of the National Academy of Sciences 103 (2): 425–430. Bibcode:2006PNAS..103..425G. doi:10.1073/pnas.0510013103. PMC 1324956. PMID 16407165. 
  95. ^ 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. doi:10.1038/msb4100050. PMC 1681482. PMID 16738554. 
  96. ^ 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 (Reading, England) 160 (Pt 11): 2341–51. doi:10.1099/mic.0.079376-0. PMID 25092907. 
  97. ^ Tu, Z; Wang, L; Xu, M; Zhou, X; Chen, T; Sun, F (21 February 2006). "Further understanding human disease genes by comparing with housekeeping genes and other genes". BMC Genomics 7: 31. doi:10.1186/1471-2164-7-31. PMC 1397819. PMID 16504025.  open access publication - free to read
  98. ^ 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. doi:10.1371/journal.pgen.1003484. PMC 3649967. PMID 23675308.  open access publication - free to read
  99. ^ Eisenberg, E; Levanon, EY (October 2013). "Human housekeeping genes, revisited.". Trends in genetics : TIG 29 (10): 569–74. doi:10.1016/j.tig.2013.05.010. PMID 23810203. 
  100. ^ Amsterdam, A; Hopkins, N (September 2006). "Mutagenesis strategies in zebrafish for identifying genes involved in development and disease.". Trends in genetics : TIG 22 (9): 473–8. doi:10.1016/j.tig.2006.06.011. PMID 16844256. 
  102. ^ Stanley N. Cohen; Annie C. Y. Chang (1 May 1973). "Recircularization and Autonomous Replication of a Sheared R-Factor DNA Segment in Escherichia coli Transformants — PNAS". Retrieved 17 July 2010. 
  103. ^ Esvelt, KM.; Wang, HH. (2013). "Genome-scale engineering for systems and synthetic biology". Mol Syst Biol 9 (1): 641. doi:10.1038/msb.2012.66. PMC 3564264. PMID 23340847. 
  105. ^ Puchta, H.; Fauser, F. (2013). "Gene targeting in plants: 25 years later". Int. J. Dev. Biol 57 (6–7–8): 629–637. doi:10.1387/ijdb.130194hp. 
  106. ^ Ran FA, Hsu PD, Wright J, Agarwala V, Scott DA, Zhang F (2013). "Genome engineering using the CRISPR-Cas9 system". Nat Protoc 8 (11): 2281–308. doi:10.1038/nprot.2013.143. PMC 3969860. PMID 24157548. 
  107. ^ Kittleson, Joshua (2012). "Successes and failures in modular genetic engineering". Current Opinion in Chemical Biology 16 (3–4): 329–336. doi:10.1016/j.cbpa.2012.06.009. PMID 22818777. 
  110. ^ Guan, Chunmei; Ye, Chao; Yang, Xiaomei; Gao, Jiangang (2010). "A review of current large-scale mouse knockout efforts". Genesis: NA. doi:10.1002/dvg.20594. 
  111. ^ Deng C (2007). "In celebration of Dr. Mario R. Capecchi's Nobel Prize". International Journal of Biological Sciences 3 (7): 417–419. doi:10.7150/ijbs.3.417. PMC 2043165. PMID 17998949. 

Further reading[edit]

External links[edit]