View source for Evolution of biological complexity

{{Short description|Tendency for maximum complexity to increase over time, though without any overall direction}}
The '''evolution of biological complexity''' is one important outcome of the process of [[evolution]].<ref>{{cite journal |last1=Werner |first1=Andreas |last2=Piatek |first2=Monica J. |last3=Mattick |first3=John S. |title=Transpositional shuffling and quality control in male germ cells to enhance evolution of complex organisms |journal=Annals of the New York Academy of Sciences |date=April 2015 |volume=1341 |issue=1 |pages=156–163 |doi=10.1111/nyas.12608 |pmid=25557795 |pmc=4390386|bibcode=2015NYASA1341..156W }}</ref> Evolution has produced some remarkably complex organisms – although the actual level of complexity is very hard to define or measure accurately in biology, with properties such as gene content, the number of [[cell type]]s or [[morphology (biology)|morphology]] all proposed as possible metrics.<ref>{{cite journal |author=Adami, C. |title=What is complexity? |journal=BioEssays |volume=24 |issue=12 |pages=1085–94 |year=2002 |pmid=12447974 |doi=10.1002/bies.10192|doi-access=free }}</ref><ref>{{cite journal |author=Waldrop, M. |title=Language: Disputed definitions |journal=Nature |volume=455 |issue=7216 |pages=1023–1028 |year=2008 |doi=10.1038/4551023a |pmid=18948925 |display-authors=etal|doi-access=free }}</ref><ref name=":0">{{Cite book |url=https://www.academia.edu/11720591 |title=Computation, Physics and Beyond |last1=Longo |first1=Giuseppe |last2=Montévil |first2=Maël |chapter=Randomness Increases Order in Biological Evolution |date=2012-01-01 |publisher=Springer Berlin Heidelberg |isbn=9783642276538 |editor-last=Dinneen |editor-first=Michael J. |series=Lecture Notes in Computer Science |volume=7160 |pages=289–308 |language=en |doi=10.1007/978-3-642-27654-5_22 |editor2-last=Khoussainov |editor2-first=Bakhadyr |editor3-last=Nies |editor3-first=André |citeseerx=10.1.1.640.1835 |s2cid=16929949 }}</ref>
Many biologists used to believe that [[Orthogenesis|evolution was progressive (orthogenesis)]] and had a direction that led towards so-called "higher organisms", despite a lack of evidence for this viewpoint.<ref>{{cite journal |author=McShea, D. |title=Complexity and evolution: What everybody knows |journal=Biology and Philosophy |volume=6 |issue=3 |pages=303–324 |year=1991 |doi=10.1007/BF00132234|s2cid=53459994 }}</ref> This idea of "progression" introduced the terms "'''high animals'''" and "'''low animals'''" in evolution. Many now regard this as misleading, with [[natural selection]] having no intrinsic direction and that organisms selected for either increased or decreased complexity in response to local environmental conditions.<ref name="Ayala">{{cite journal |author=Ayala, F. J. |title=Darwin's greatest discovery: design without designer |journal=PNAS |volume=104 |issue= Suppl 1|pages=8567–73 |year=2007 |pmid=17494753 |doi=10.1073/pnas.0701072104 |pmc=1876431|bibcode=2007PNAS..104.8567A |doi-access=free }}</ref> Although there has been an increase in the maximum level of complexity over the [[history of life]], there has always been a large majority of small and simple organisms and the [[mode (statistics)|most common]] level of complexity appears to have remained relatively constant.
==Selection for simplicity and complexity==
Usually organisms that have a higher rate of reproduction than their competitors have an evolutionary advantage. Consequently, organisms can evolve to become simpler and thus multiply faster and produce more offspring, as they require fewer resources to reproduce. A good example are parasites such as ''Plasmodium'' – the parasite responsible for [[malaria]] – and [[mycoplasma]]; these organisms often dispense with traits that are made unnecessary through parasitism on a host.<ref>{{cite journal |author1=Sirand-Pugnet, P. |author2=Lartigue, C. |author3=Marenda, M.  |title=Being Pathogenic, Plastic, and Sexual while Living with a Nearly Minimal Bacterial Genome |journal=PLOS Genet. |volume=3 |issue=5 |pages=e75 |year=2007 |pmid=17511520 |doi=10.1371/journal.pgen.0030075 |pmc=1868952 |display-authors=etal |doi-access=free }}</ref>
A lineage can also dispense with complexity when a particular complex trait merely provides no selective advantage in a particular environment. Loss of this trait need not necessarily confer a selective advantage, but may be lost due to the accumulation of mutations if its loss does not confer an immediate selective disadvantage.<ref>{{cite journal |author1=Maughan, H. |author2=Masel, J. |author3=Birky, W. C. |author4=Nicholson, W. L.  |title=The roles of mutation accumulation and selection in loss of sporulation in experimental populations of Bacillus subtilis |doi=10.1534/genetics.107.075663 |journal=Genetics |volume=177 |pages=937–948 |year=2007 |pmid=17720926 |pmc=2034656 |issue=2}}</ref> For example, a [[parasitic organisms|parasitic organism]] may dispense with the synthetic pathway of a metabolite where it can readily scavenge that metabolite from its host. Discarding this synthesis may not necessarily allow the parasite to conserve significant energy or resources and grow faster, but the loss may be fixed in the population through mutation accumulation if no disadvantage is incurred by loss of that pathway. Mutations causing loss of a complex trait occur more often than mutations causing gain of a complex trait.{{citation needed|date=April 2020}}
With selection, evolution can also produce more complex organisms. Complexity often arises in the co-evolution of hosts and pathogens,<ref name="arms_race">{{cite journal |author1=Dawkins, Richard  |author1-link=Richard Dawkins |author2=Krebs, J. R. |title=Arms Races between and within Species |journal=[[Proceedings of the Royal Society B]] |volume=205 |issue=1161 |pages=489–511 |year=1979 |doi=10.1098/rspb.1979.0081 |pmid=42057 |bibcode=1979RSPSB.205..489D |s2cid=9695900 }}</ref> with each side developing ever more sophisticated adaptations, such as the [[immune system]] and the many techniques pathogens have developed to evade it. For example, the parasite ''[[Trypanosoma brucei]]'', which causes [[African trypanosomiasis|sleeping sickness]], has evolved so many copies of its major surface [[antigen]] that about 10% of its genome is devoted to different versions of this one gene. This tremendous complexity allows the parasite to constantly change its surface and thus evade the immune system through [[antigenic variation]].<ref>{{cite journal |author=Pays, E. |title=Regulation of antigen gene expression in Trypanosoma brucei |journal=Trends Parasitol. |volume=21 |issue=11 |pages=517–20 |year=2005 |pmid=16126458 |doi=10.1016/j.pt.2005.08.016}}</ref>
More generally, the growth of complexity may be driven by the [[co-evolution]] between an organism and the [[ecosystem]] of [[predator]]s, [[prey]] and [[parasite]]s to which it tries to stay adapted: as any of these become more complex in order to cope better with the diversity of threats offered by the ecosystem formed by the others, the others too will have to adapt by becoming more complex, thus triggering an ongoing [[evolutionary arms race]]<ref name="arms_race"/> towards more complexity.<ref>[[Francis Heylighen|Heylighen, F.]] (1999a) [https://books.google.com/books?id=BQWrppy8ooIC&dq=%22Heylighen%22+%22The+growth+of+structural+and+functional+complexity+...%22+&pg=PA17 "The Growth of Structural and Functional Complexity during Evolution]", in F. Heylighen, J. Bollen & A. Riegler (eds.) The Evolution of Complexity Kluwer Academic, Dordrecht, 17–44.</ref> This trend may be reinforced by the fact that ecosystems themselves tend to become more complex over time, as [[species diversity]] increases, together with the linkages or dependencies between species.
==Types of trends in complexity==
[[File:Evolution of complexity.svg|thumb|left|200px|Passive versus active trends in complexity. Organisms at the beginning are red. Numbers are shown by height with time moving up in a series.]]
If evolution possessed an active trend toward complexity ([[orthogenesis]]), as was widely believed in the 19th century,<ref>{{cite book |last=Ruse |first=Michael |author-link=Michael Ruse |date=1996 |title=Monad to man: the Concept of Progress in Evolutionary Biology |url=https://archive.org/details/monadtomanconcep0000ruse |url-access=registration |publisher=Harvard University Press |isbn=978-0-674-03248-4 |pages=[https://archive.org/details/monadtomanconcep0000ruse/page/526 526]–529 and passim}}</ref> then we would expect to see an active trend<!--right hand column in figure--> of increase over time in the most common value [[mode (statistics)|(the mode)]] of complexity among organisms.<ref name=Carroll>{{cite journal |author=Carroll SB |title=Chance and necessity: the evolution of morphological complexity and diversity |journal=Nature |volume=409 |issue=6823 |pages=1102–9 |year=2001 |pmid=11234024 |doi=10.1038/35059227|bibcode=2001Natur.409.1102C |s2cid=4319886 }}</ref>
However, an increase in complexity can also be explained through a passive process.<ref name=Carroll/> Assuming unbiased random changes of complexity and the existence of a minimum complexity leads to an increase over time of the average complexity of the biosphere. This involves an increase in [[variance]], but the mode does not change. The trend towards the creation of some organisms with higher complexity over time exists, but it involves increasingly small percentages of living things.<ref name=":0" />
In this hypothesis, any appearance of evolution acting with an intrinsic direction towards increasingly complex organisms is a result of people concentrating on the small number of large, complex organisms that inhabit the [[Skewness|right-hand tail]] of the complexity distribution and ignoring simpler and much more common organisms. This passive model predicts that the majority of species are [[microorganism|microscopic]] [[prokaryote]]s, which is supported by estimates of 10<sup>6</sup> to 10<sup>9</sup> extant prokaryotes<ref>{{cite journal |author=Oren, A. |title=Prokaryote diversity and taxonomy: current status and future challenges |journal=Philos. Trans. R. Soc. Lond. B Biol. Sci. |volume=359 |issue=1444 |pages=623–38 |year=2004 |pmid=15253349 |doi=10.1098/rstb.2003.1458 |pmc=1693353}}</ref> compared to diversity estimates of 10<sup>6</sup> to 3·10<sup>6</sup> for eukaryotes.<ref>{{cite journal |title=How Many Species? |journal= Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences|doi=10.1098/rstb.1990.0200 |year=1990 |last1=May |first1=R. M. |last2=Beverton |first2=R. J. H. |volume=330 |pages=293–304 |issue=1257}}</ref><ref>{{cite journal |author1=Schloss, P. |author2=Handelsman, J.  |title=Status of the microbial census |journal=Microbiol Mol Biol Rev |volume=68 |issue=4 |pages=686–91 |year=2004 |pmid=15590780 |doi=10.1128/MMBR.68.4.686-691.2004 |pmc=539005}}</ref> Consequently, in this view, microscopic life dominates Earth, and large organisms only appear more diverse due to [[sampling bias]].
Genome complexity has generally increased since the beginning of the life on Earth.<ref>{{cite journal | last1=Markov | first1=A. V. | last2=Anisimov | first2=V. A. | last3=Korotayev | first3=A. V. | year=2010 | title=Relationship between genome size and organismal complexity in the lineage leading from prokaryotes to mammals | journal=Paleontological Journal | volume=44 | issue=4| pages=363–373 | doi=10.1134/s0031030110040015| bibcode=2010PalJ...44..363M | s2cid=10830340 }}</ref><ref>{{cite journal | last1=Sharov | first1=Alexei A | year=2006 | title=Genome increase as a clock for the origin and evolution of life | doi=10.1186/1745-6150-1-17 | pmid=16768805 | pmc=1526419 | journal=Biology Direct | volume=1 | issue=1| page=17 | doi-access=free }}</ref> Some [[artificial life|computer models]] have suggested that the generation of complex organisms is an inescapable feature of evolution.<ref>{{cite journal |author1=Furusawa, C. |author2=Kaneko, K.  |title=Origin of complexity in multicellular organisms |journal=Phys. Rev. Lett. |volume=84 |issue=26 Pt 1 |pages=6130–3 |year=2000 |pmid=10991141 |doi=10.1103/PhysRevLett.84.6130 |bibcode=2000PhRvL..84.6130F|arxiv=nlin/0009008 |s2cid=13985096 }}</ref><ref>{{cite journal |author1=Adami, C. |author2=Ofria, C. |author3=Collier, T. C.  |title=Evolution of biological complexity |journal=PNAS |volume=97 |issue=9 |pages=4463–8 |year=2000 |pmid=10781045 |doi=10.1073/pnas.97.9.4463 |pmc=18257 |arxiv=physics/0005074 |bibcode=2000PNAS...97.4463A |doi-access=free }}</ref> Proteins tend to become more hydrophobic over time,<ref>{{cite journal |last1=Wilson |first1=Benjamin A. |last2=Foy |first2=Scott G. |last3=Neme |first3=Rafik |last4=Masel |first4=Joanna |title=Young genes are highly disordered as predicted by the preadaptation hypothesis of de novo gene birth |journal=Nature Ecology & Evolution |date=24 April 2017 |volume=1 |issue=6 |pages=0146–146 |doi=10.1038/s41559-017-0146|pmid=28642936 |pmc=5476217 |bibcode=2017NatEE...1..146W }}</ref> and to have their hydrophobic amino acids more interspersed along the primary sequence.<ref>{{cite journal |last1=Foy |first1=Scott G. |last2=Wilson |first2=Benjamin A. |last3=Bertram |first3=Jason |last4=Cordes |first4=Matthew H. J. |last5=Masel |first5=Joanna |title=A Shift in Aggregation Avoidance Strategy Marks a Long-Term Direction to Protein Evolution |journal=Genetics |date=April 2019 |volume=211 |issue=4 |pages=1345–1355 |doi=10.1534/genetics.118.301719|pmid=30692195 |pmc=6456324 }}</ref> Increases in body size over time are sometimes seen in what is known as [[Cope's rule]].<ref>{{cite journal | last1=Heim | first1=N. A. | last2=Knope | first2=M. L. | last3=Schaal | first3=E. K. | last4=Wang | first4=S. C. | last5=Payne | first5=J. L.  | title=Cope's rule in the evolution of marine animals | journal=Science | volume=347 | issue=6224 | pages=867–870 | doi=10.1126/science.1260065 | date=2015-02-20 |bibcode=2015Sci...347..867H | pmid=25700517| doi-access=free }}</ref>
==Constructive neutral evolution==
{{Further|Constructive neutral evolution}}
Recently work in evolution theory has proposed that by relaxing [[selection pressure]], which typically acts to streamline [[genome]]s, the complexity of an organism increases by a process called [[constructive neutral evolution]].<ref name="Stoltzfus1999">{{cite journal |last1=Stoltzfus |first1=Arlin |title=On the Possibility of Constructive Neutral Evolution |journal=Journal of Molecular Evolution |volume=49 |issue=2 |year=1999 |pages=169–181 |doi=10.1007/PL00006540|pmid=10441669 |issn=0022-2844|bibcode=1999JMolE..49..169S |citeseerx=10.1.1.466.5042 |s2cid=1743092 }}</ref> Since the [[effective population size]] in eukaryotes (especially multi-cellular organisms) is much smaller than in prokaryotes,<ref name="SungAckerman2012">{{cite journal |last1=Sung |first1=W. |last2=Ackerman |first2=M. S. |last3=Miller |first3=S. F. |last4=Doak |first4=T. G. |last5=Lynch |first5=M. |title=Drift-barrier hypothesis and mutation-rate evolution |journal=Proceedings of the National Academy of Sciences |volume=109 |issue=45 |year=2012 |pages=18488–18492 |doi=10.1073/pnas.1216223109|pmc=3494944 |bibcode=2012PNAS..10918488S |pmid=23077252|doi-access=free }}</ref> they experience [[nearly neutral theory of molecular evolution|lower selection constraints]].
According to this model, new genes are created by non-[[adaptation (biology)|adaptive]] processes, such as by random [[gene duplication]]. These novel entities, although not required for viability, do give the organism excess capacity that can facilitate the mutational decay of functional subunits. If this decay results in a situation where all of the genes are now required, the organism has been trapped in a new state where the number of genes has increased. This process has been sometimes described as a complexifying ratchet.<ref name="LukešArchibald2011">{{cite journal |last1=Lukeš |first1=Julius |last2=Archibald |first2=John M. |last3=Keeling |first3=Patrick J. |last4=Doolittle |first4=W. Ford |last5=Gray |first5=Michael W. |title=How a neutral evolutionary ratchet can build cellular complexity |journal=IUBMB Life |volume=63 |issue=7 |year=2011 |pages=528–537 |doi=10.1002/iub.489|pmid=21698757 |s2cid=7306575 |doi-access=free }}</ref> These supplemental genes can then be co-opted by natural selection by a process called [[neofunctionalization]]. In other instances constructive neutral evolution does not promote the creation of new parts, but rather promotes novel interactions between existing players, which then take on new moonlighting roles.<ref name="LukešArchibald2011"/>
Constructive neutral evolution has also been used to explain how ancient complexes, such as the [[spliceosome]] and the [[ribosome]], have gained new subunits over time, how new alternative spliced isoforms of genes arise, how [[Ciliate#DNA rearrangements (gene scrambling)|gene scrambling]] in [[ciliates]] evolved, how pervasive pan-[[RNA editing]] may have arisen in ''[[Trypanosoma brucei]]'', how functional [[lncRNA]]s have likely arisen from transcriptional noise, and how even useless protein complexes can persist for millions of years.<ref name="Stoltzfus1999"/><ref name="GrayLukes2010">{{cite journal |last1=Gray |first1=M. W. |last2=Lukes |first2=J. |last3=Archibald |first3=J. M. |last4=Keeling |first4=P. J. |last5=Doolittle |first5=W. F. |title=Irremediable Complexity? |journal=Science |volume=330 |issue=6006 |year=2010 |pages=920–921 |issn=0036-8075 |doi=10.1126/science.1198594|pmid=21071654 |bibcode=2010Sci...330..920G |s2cid=206530279 }}</ref><ref name="LukešArchibald2011"/><ref name="DanielBehm2015">{{cite journal |last1=Daniel |first1=Chammiran |last2=Behm |first2=Mikaela |last3=Öhman |first3=Marie |title=The role of Alu elements in the cis-regulation of RNA processing |journal=Cellular and Molecular Life Sciences |volume=72 |issue=21 |year=2015 |pages=4063–4076 |issn=1420-682X |doi=10.1007/s00018-015-1990-3|pmid=26223268 |s2cid=17960570 |pmc=11113721 }}</ref><ref name="CovelloGray1993">{{cite journal |last1=Covello |first1=PatrickS. |last2=Gray |first2=MichaelW. |title=On the evolution of RNA editing |journal=Trends in Genetics |volume=9 |issue=8 |year=1993 |pages=265–268 |doi=10.1016/0168-9525(93)90011-6|pmid=8379005 }}</ref><ref name="PalazzoKoonin2020">{{cite journal|last1=Palazzo|first1=Alexander F.|last2=Koonin|first2=Eugene V.|title=Functional Long Non-coding RNAs Evolve from Junk Transcripts|journal=Cell|volume=183|issue=5|year=2020|pages=1151–1161|issn=0092-8674|doi=10.1016/j.cell.2020.09.047|pmid=33068526|s2cid=222815635|doi-access=free}}</ref><ref>{{cite journal |last1=Hochberg |first1=GKA |last2=Liu |first2=Y |last3=Marklund |first3=EG |last4=Metzger |first4=BPH |last5=Laganowsky |first5=A |last6=Thornton |first6=JW |title=A hydrophobic ratchet entrenches molecular complexes. |journal=Nature |date=December 2020 |volume=588 |issue=7838 |pages=503–508 |doi=10.1038/s41586-020-3021-2 |pmid=33299178|pmc=8168016 |bibcode=2020Natur.588..503H }}</ref>
== Mutational hazard hypothesis ==
The mutational hazard hypothesis is a non-adaptive theory for increased complexity in genomes.<ref name=":1">{{Cite journal|last1=Lynch|first1=Michael|last2=Conery|first2=John S.|date=2003-11-21|title=The Origins of Genome Complexity|url=https://www.science.org/doi/10.1126/science.1089370|journal=Science|language=en|volume=302|issue=5649|pages=1401–1404|doi=10.1126/science.1089370|pmid=14631042|bibcode=2003Sci...302.1401L |s2cid=11246091|issn=0036-8075}}</ref> The basis of mutational hazard hypothesis is that each mutation for [[non-coding DNA]] imposes a fitness cost.<ref name=":2">{{Cite journal|last1=Lynch|first1=Michael|last2=Bobay|first2=Louis-Marie|last3=Catania|first3=Francesco|last4=Gout|first4=Jean-François|last5=Rho|first5=Mina|date=2011-09-22|title=The Repatterning of Eukaryotic Genomes by Random Genetic Drift|journal=Annual Review of Genomics and Human Genetics|language=en|volume=12|issue=1|pages=347–366|doi=10.1146/annurev-genom-082410-101412|issn=1527-8204|pmc=4519033|pmid=21756106}}</ref> Variation in complexity can be described by 2N<sub>e</sub>u, where N<sub>e</sub> is effective population size and u is [[mutation rate]].<ref name=":3">{{Cite journal|last=Lynch|first=M.|date=2006-03-24|title=Mutation Pressure and the Evolution of Organelle Genomic Architecture|url=https://www.science.org/doi/10.1126/science.1118884|journal=Science|language=en|volume=311|issue=5768|pages=1727–1730|doi=10.1126/science.1118884|pmid=16556832|bibcode=2006Sci...311.1727L |s2cid=2678365|issn=0036-8075}}</ref>
In this hypothesis, selection against non-coding DNA can be reduced in three ways: random genetic drift, recombination rate, and mutation rate.<ref name=":4">{{Cite journal|last=Lynch|first=Michael|date=2006-02-01|title=The Origins of Eukaryotic Gene Structure|url=http://academic.oup.com/mbe/article/23/2/450/1119102/The-Origins-of-Eukaryotic-Gene-Structure|journal=Molecular Biology and Evolution|language=en|volume=23|issue=2|pages=450–468|doi=10.1093/molbev/msj050|pmid=16280547|issn=1537-1719|doi-access=free}}</ref> As complexity increases from prokaryotes to multicellular eukaryotes, [[effective population size]] decreases, subsequently increasing the strength of [[Genetic drift|random genetic drift]].<ref name=":1" />  This, along with low recombination rate<ref name=":4" /> and high mutation rate,<ref name=":4" /> allows non-coding DNA to proliferate without being removed by [[Negative selection (natural selection)|purifying selection]].<ref name=":1" />
Accumulation of non-coding DNA in larger genomes can be seen when comparing genome size and genome content across eukaryotic taxa. There is a positive correlation between genome size and noncoding DNA genome content with each group staying within some variation.<ref name=":1" /><ref name=":2" /> When comparing variation in complexity in organelles, effective population size is replaced with genetic effective population size (N<sub>g</sub>).<ref name=":3" /> If looking at [[Silent mutation|silent-site]] nucleotide diversity, then larger genomes are expected to have less diversity than more compact ones. In plant and animal [[Mitochondrion|mitochondria]], differences in mutation rate account for the opposite directions in complexity, with plant mitochondria being more complex and animal mitochondria more streamlined.<ref>{{Cite journal|last=Lynch|first=Michael|date=2006-10-13|title=Streamlining and Simplification of Microbial Genome Architecture|url=http://www.annualreviews.org/doi/10.1146/annurev.micro.60.080805.142300|journal=Annual Review of Microbiology|language=en|volume=60|issue=1|pages=327–349|doi=10.1146/annurev.micro.60.080805.142300|pmid=16824010|issn=0066-4227}}</ref>
The mutational hazard hypothesis has been used to at least partially explain expanded genomes in some species. For example, when comparing ''[[Volvox carteri|Volvox cateri]]'' to a close relative with a compact genome, ''[[Chlamydomonas reinhardtii]]'', the former had less silent-site diversity than the latter in nuclear, mitochondrial, and plastid genomes.<ref>{{Cite journal|last1=Smith|first1=D. R.|last2=Lee|first2=R. W.|date=2010-10-01|title=Low Nucleotide Diversity for the Expanded Organelle and Nuclear Genomes of Volvox carteri Supports the Mutational-Hazard Hypothesis|url=https://academic.oup.com/mbe/article-lookup/doi/10.1093/molbev/msq110|journal=Molecular Biology and Evolution|language=en|volume=27|issue=10|pages=2244–2256|doi=10.1093/molbev/msq110|pmid=20430860|issn=0737-4038|doi-access=free}}</ref> However, when comparing the plastid genome of ''[[Volvox carteri|Volvox cateri]]'' to ''[[Volvox|Volvox africanus]]'', a species in the same genus but with half the plastid genome size, there were high mutation rates in intergenic regions.<ref>{{Cite journal|last1=Gaouda|first1=Hager|last2=Hamaji|first2=Takashi|last3=Yamamoto|first3=Kayoko|last4=Kawai-Toyooka|first4=Hiroko|last5=Suzuki|first5=Masahiro|last6=Noguchi|first6=Hideki|last7=Minakuchi|first7=Yohei|last8=Toyoda|first8=Atsushi|last9=Fujiyama|first9=Asao|last10=Nozaki|first10=Hisayoshi|last11=Smith|first11=David Roy|date=2018-09-01|editor-last=Chaw|editor-first=Shu-Miaw|title=Exploring the Limits and Causes of Plastid Genome Expansion in Volvocine Green Algae|url= |journal=Genome Biology and Evolution|language=en|volume=10|issue=9|pages=2248–2254|doi=10.1093/gbe/evy175|issn=1759-6653|pmc=6128376|pmid=30102347}}</ref> In ''[[Arabidopsis thaliana|Arabiopsis thaliana]],'' the hypothesis was used as a possible explanation for intron loss and compact genome size. When compared to ''[[Arabidopsis lyrata]]'', researchers found a higher mutation rate overall and in lost introns (an intron that is no longer transcribed or spliced) compared to conserved introns.<ref>{{Cite journal|last1=Yang|first1=Yu-Fei|last2=Zhu|first2=Tao|last3=Niu|first3=Deng-Ke|date=April 2013|title=Association of Intron Loss with High Mutation Rate in Arabidopsis: Implications for Genome Size Evolution|url= |journal=Genome Biology and Evolution|language=en|volume=5|issue=4|pages=723–733|doi=10.1093/gbe/evt043|issn=1759-6653|pmc=4104619|pmid=23516254}}</ref>
There are expanded genomes in other species that could not be explained by the mutational hazard hypothesis. For example, the expanded mitochondrial genomes of ''[[Silene noctiflora]]'' and ''[[Silene conica]]'' have high mutation rates, lower intron lengths, and more non-coding DNA elements compared to others in the same genus, but there was no evidence for long-term low effective population size.<ref>{{Cite journal|last1=Sloan|first1=Daniel B.|last2=Alverson|first2=Andrew J.|last3=Chuckalovcak|first3=John P.|last4=Wu|first4=Martin|last5=McCauley|first5=David E.|last6=Palmer|first6=Jeffrey D.|last7=Taylor|first7=Douglas R.|date=2012-01-17|editor-last=Gray|editor-first=Michael William|title=Rapid Evolution of Enormous, Multichromosomal Genomes in Flowering Plant Mitochondria with Exceptionally High Mutation Rates|journal=PLOS Biology|language=en|volume=10|issue=1|pages=e1001241|doi=10.1371/journal.pbio.1001241|issn=1545-7885|pmc=3260318|pmid=22272183 |doi-access=free }}</ref> The mitochondrial genomes of ''[[Watermelon|Citrullus lanatus]]'' and ''[[Cucurbita pepo]]'' differ in several ways. ''[[Watermelon|Citrullus lanatus]]'' is smaller, has more introns and duplications, while ''[[Cucurbita pepo]]'' is larger with more chloroplast and short repeated sequences.<ref name=":5">{{Cite journal|last1=Alverson|first1=Andrew J|last2=Wei|first2=XioXin|last3=Rice|first3=Danny W|last4=Stern|first4=David B|last5=Barry|first5=Kerrie|last6=Palmer|first6=Jeffrey D|date=2010-01-29|title=Insights into the Evolution of Mitochondrial Genome Size from Complete Sequences of Citrus lanatus and Cucurbita pepo (Cucurbitaceae)|journal=Molecular Biology and Evolution|volume=27|issue=6|pages=1436–1448|doi=10.1093/molbev/msq029|pmid=20118192|pmc=2877997}}</ref> If [[RNA editing]] sites and mutation rate lined up, then ''[[Cucurbita pepo]]'' would have a lower mutation rate and more RNA editing sites. However the mutation rate is four times higher than ''[[Watermelon|Citrullus lanatus]]'' and they have a similar number of RNA editing sites.<ref name=":5" /> There was also an attempt to use the hypothesis to explain large nuclear genomes of [[salamander]]s, but researchers found opposite results than expected, including lower long-term strength of genetic drift.<ref>{{Cite journal|last1=Mohlhenrich|first1=Erik Roger|last2=Lockridge Mueller|first2=Rachel|date=2016-09-27|title=Genetic drift and mutational hazard in the evolution of salamander genomic gigantism|journal=Evolution|volume=70|issue=12|pages=2865–2878|doi=10.1111/evo.13084|pmid=27714793|hdl=10217/173461|s2cid=205125025|via=JSTOR|hdl-access=free}}</ref>
==History==
{{further|Orthogenesis}}
In the 19th century, some scientists such as [[Jean-Baptiste Lamarck]] (1744–1829) and [[Ray Lankester]] (1847–1929) believed that nature had an innate striving to become more complex with evolution. This belief may reflect then-current ideas of [[Georg Wilhelm Friedrich Hegel|Hegel]] (1770–1831) and of [[Herbert Spencer]] (1820–1903) which envisaged the universe gradually evolving to a higher, more perfect state.
This view regarded the evolution of parasites from independent organisms to a parasitic species as "[[Devolution (biology)|devolution]]" or "degeneration", and contrary to nature. Social theorists have sometimes interpreted this approach metaphorically to decry certain categories of people as "degenerate parasites". Later scientists regarded biological devolution as nonsense; rather, lineages become simpler or more complicated according to whatever forms had a selective advantage.<ref>{{cite journal |author=Dougherty, Michael J. | title=Is the human race evolving or devolving? | url=http://www.scientificamerican.com/article/is-the-human-race-evolvin/ | journal=Scientific American |date=July 1998 | quote=From a biological perspective, there is no such thing as devolution. All changes in the gene frequencies of populations—and quite often in the traits those genes influence—are by definition evolutionary changes. [...] When species do evolve, it is not out of need but rather because their populations contain organisms with variants of traits that offer a reproductive advantage in a changing environment.}}</ref>
In a 1964 book, The Emergence of Biological Organization, [[Henry Quastler|Quastler]] pioneered a theory of emergence, developing a model of a series of emergences from protobiological systems to prokaryotes without the need to invoke implausible very low probability events.<ref>Quastler, H. (1964) The Emergence of Biological Organization. Yale University Press</ref>
The evolution of order, manifested as biological complexity, in living systems and the generation of order in certain non-living systems was proposed in 1983 to obey a common fundamental principal called “the Darwinian dynamic”.<ref>Bernstein H, Byerly HC, Hopf FA, Michod RA, Vemulapalli GK. (1983) The Darwinian Dynamic. Quarterly Review of Biology 58, 185-207. JSTOR 2828805</ref>  The Darwinian dynamic was formulated by first considering how microscopic order is generated in simple non-biological systems that are far from [[thermodynamic equilibrium]].  Consideration was then extended to short, replicating [[RNA]] molecules assumed to be similar to the earliest forms of life in the [[RNA world]].  It was shown that the underlying order-generating processes in the non-biological systems and in replicating RNA are basically similar.  This approach helped clarify the relationship of thermodynamics to evolution as well as the empirical content of [[Charles Darwin|Darwin]]'s theory.
In 1985, [[Harold J. Morowitz|Morowitz]]<ref>{{Cite book |last=Morowitz |first=Harold J. |title=Mayonnaise and the origin of life: thoughts of minds and molecules |date=1985 |publisher=Scribner |isbn=978-0-684-18444-9 |location=New York}}</ref> noted that the modern era of [[Non-equilibrium thermodynamics|irreversible thermodynamics]] ushered in by [[Lars Onsager]] in the 1930s showed that systems invariably become ordered under a flow of energy, thus indicating that the existence of life involves no contradiction to the laws of physics.
==See also==
{{div col|colwidth=30}}
* [[Biocomplexity]]
* [[Biodiversity]]
* [[Biosphere]]
* [[Complex adaptive system]]
* [[Complex systems biology]]
* [[Constructive neutral evolution]]
* [[Dual-phase evolution]]
* [[Ecosystem]]
* [[Evolutionary trade-offs]]
* [[Evolvability]]
{{div col end}}
==References==
{{reflist|30em}}
{{evolution}}
[[Category:Evolutionary biology]]
[[Category:Evolution by phenotype|Complexity]]