Evolutionary tinkering

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Evolutionary tinkering is an explanation of how evolution happens in nature. It explains that evolution works as a tinkerer who experiments with miscellaneous items, unsure of the outcome, and utilizes whatever is available to craft functional objects whose utility may only become evident later. None of the materials serve a defined purpose initially, and each can be employed in multiple ways. According to the tinkering concept, “evolution does not produce novelties from scratch". [1] It comes from previously unseen associations of old materials to modify an existing system to give a new function or combine systems together to enhance the functions. [2] The transformation from unicellular to multicellular during evolution is such an event which has elaborated the existing function.

Contents

The process of evolutionary tinkering takes quite a long time. As a meticulous tinkerer who continuously refines its creations, making adjustments, trimming and extending here and there, seizing every chance to gradually tailor them to their evolving purposes, this process happens over countless eons. [1]

Most of the time, traits in nature are barely favorable enough for organisms to survive. For instance, RuBisCO is profoundly inefficient, despite the fact that it catalyzes one of the most important reactions on the planet: carbon fixation. This is likely due to the enzyme originating in the common ancestor of all plastids when the atmospheric conditions were drastically different than they are today. [3]

François Jacob

In his seminal article 'Evolution and Tinkering', [1] François Jacob first introduced the idea of tinkering to a broad audience of scientists, drawing from diverse fields such as molecular biology, evolutionary biology, and cultural anthropology. The concept of tinkering, or more precisely, the notion of bricolage, serves as a theoretical framework for analyzing various phenomena characterized by a common underlying process: the opportunistic rearrangement and recombination of existing elements. Jacob and Monad also won the Nobel Prize in 1965 for his work on the lac operon. [4]

Engineering versus tinkering

Natural selection is frequently likened to the work of an engineer, yet this analogy falls short. [5] Unlike the engineer who operates based on meticulous planning and a clear vision of the end product, evolution lacks such deliberate intent. [6] Additionally, while the engineer has access to carefully selected materials and specialized equipment tailored for their tasks, evolution relies on the resources available in its surroundings.

Moreover, the engineer's creations tend to approach a level of perfection achievable with current technology, whereas evolution does not strive for perfection but rather resembles a tinkerer. This tinkerer, akin to evolution, lacks a precise blueprint of the outcome and instead utilizes whatever materials are at hand to fashion something functional. While the engineer depends on specific materials and tools precisely suited to their project, the tinkerer makes do with miscellaneous scraps and remnants. The resulting creations of the tinkerer emerge from a series of opportunistic events, enriching their repertoire with each encounter.

The development of lungs in terrestrial vertebrates illustrates a process akin to tinkering rather than deliberate engineering. It originated in certain freshwater fish faced with oxygen deficient environments, leading them to ingest air and absorb oxygen through their esophageal walls. Over time, this behavior favored the enlargement of the esophageal surface area, eventually giving rise to lung-like structures through the emergence and enlargement of esophageal diverticula. [7]

The brain is the key adaptive feature of humans, yet still holds mysteries regarding its precise purpose. The brain has also evolved through natural selection over millions of years, like other body parts, primarily to serve our reproductive needs. However, the human brain's development was more complex unlike straightforward evolutionary changes such as a leg into a wing. It involved adding new structures, particularly the neocortex, onto older ones. This rapid evolution led to a division between the neocortex, responsible for intellectual functions, and the older structures, controlling emotional and visceral activities. These older structures lack the discriminative and symbolic abilities of the neocortex and are primarily associated with emotions. Despite the dominance of the neocortex in intellectual processes, the older structures maintain strong connections with automatic centers, ensuring vital functions like obtaining food and responding to threats. This evolutionary process, characterized by the emergence of a dominant neocortex alongside the persistence of older systems, resembles a tinkering process, where new elements are added onto existing ones without fully replacing them. [8]

Evolution by molecular tinkering

Jacob was convinced that although morphological analysis supports his notion of bricolage, one would find more evidence of tinkering at the molecular level. [1] [9] The tinkering model suggests that the genes of the earliest organisms were very short, and all subsequent genes were formed by duplication, combination, and reassorting these original sequences. [9] [10] It is well established that gene duplication has produced a great deal of diversity throughout evolutionary history. [11] One example of molecular tinkering can be found in mitochondrial nucleoproteins, some of which originate from eukaryotes; in this case, the tinkerer used whatever tools were at her disposal, including materials from an entirely different taxonomic domain. [12]

To understand molecular tinkering, it is important to grasp the concept of a protein domain, which is a distinct region of a protein that has a defined shape, which determines the function of the protein. [3] Some have used the analogy of Lego blocks to explain: the domains can be taken apart and put together again in unique ways, thus changing the shape and function of the protein. [13] There are many different means by which tinkering can result in molecular and phenotypic novelty, primarily by taking apart the Lego blocks of proteins and putting them together again in unique patterns. Generally, these processes add to the organizational complexity of the genome, the proteome, or both. [3]

Internal gene duplication

There are several forms of gene duplication. The product of whole-gene duplication is two copies of the gene, whereas that of diploid-type gene duplication is one gene that has doubled in length. Internal gene duplication results in repeated nucleotide sequences within a gene, and less than 100% of the gene is replicated. [3] Because adding nucleotides to a sequence could impact splicing, this process may result in changing the identity of introns and exons; alternatively, the sequence may retain its original identity as an exon or intron, respectively. [3] If an exon that encodes for one or more domains is duplicated, this could directly result in a more complex protein via domain accretion. [3] [14] [15] Eukaryotic genes have undergone frequent internal gene duplication throughout evolutionary history. [16] One example is seen in the dinucleotide-binding regions of glyceraldehyde 3-phosphate dehydrogenase and alcohol dehydrogenase: the duplicated domain is capable of binding with more molecules than the unduplicated. [3] Another is the ovomucoid gene, which is the product of two internal duplications. [3]

Mosaic proteins

Mosaic proteins are encoded by chimeric genes (or mosaic genes). These genes result from domain shuffling, which is accomplished via exon shuffling, gene fusion, or gene fission. [3] Domain shuffling has been found to be at least partially responsible for some traits in modern vertebrates. [17] Most domains only have a small number of uses, while very few domains are used as Lego blocks over and over again in multidomain proteins. [3] Phenotypic innovation does not arise solely from the creation of new proteins, but also from changing gene expression and protein-protein interactions. [3] One example of novelty associated with domain shuffling is multicellularity. [3]

Gene fusion (the creation of a fusion gene by joining two genes together) and gene fission or fragmentation, which results in splitting one gene with many domains into multiple smaller genes, are the other two molecular mechanisms by which mosaic proteins can be formed. [3]

Alternative splicing

Alternative splicing is another mechanism of molecular tinkering that may be responsible for increasing diversity in the proteome. [3] One special kind of alternative splicing is nested genes, which produce intron-encoded proteins. [3] It has been proposed that nested gene structures could be maintained via neutral processes [3] according to the neutral theory of evolution.

De novo evolution of protein-coding genes from non-coding DNA

De novo gene birth is very rare. The most probable path from noncoding DNA to a protein-coding gene is to first become a protogene, similar to how functional genes first become pseudogenes before becoming completely nongenic. [3] Although they are too rare to notably increase the number of proteins in a given lineage, the tinkering model posits that adding just a few Lego blocks to the collection allows for many new possible combinations of domains, i.e., proteins with new shapes and functions. [3]

Exonization of introns and pseudoexonization of exons

Exonization is a very rare phenomenon in which an intron becomes an exon. [3] In pseudoexonization, an exon becomes nonfunctional; this in turn changes the shape and function of the protein. [3]

Gene loss and unitary pseudogenes

When selective constraints disappear, it is possible for genes to be lost via one of two mechanisms. The first is deleting a single-copy gene. [3] The second is nonfunctionalization of a single-copy gene; this produces a unitary pseudogene, which has no functional paralogs, is comparable to vestigial anatomical structures, and is uncommon due to its often deleterious nature. [3] In the rare case that gene loss becomes fixed in a population, it is difficult to definitively say what was the cause.

Related Research Articles

<span class="mw-page-title-main">Exon</span> A region of a transcribed gene present in the final functional mRNA molecule

An exon is any part of a gene that will form a part of the final mature RNA produced by that gene after introns have been removed by RNA splicing. The term exon refers to both the DNA sequence within a gene and to the corresponding sequence in RNA transcripts. In RNA splicing, introns are removed and exons are covalently joined to one another as part of generating the mature RNA. Just as the entire set of genes for a species constitutes the genome, the entire set of exons constitutes the exome.

An intron is any nucleotide sequence within a gene that is not expressed or operative in the final RNA product. The word intron is derived from the term intragenic region, i.e., a region inside a gene. The term intron refers to both the DNA sequence within a gene and the corresponding RNA sequence in RNA transcripts. The non-intron sequences that become joined by this RNA processing to form the mature RNA are called exons.

<span class="mw-page-title-main">RNA splicing</span> Process in molecular biology

RNA splicing is a process in molecular biology where a newly-made precursor messenger RNA (pre-mRNA) transcript is transformed into a mature messenger RNA (mRNA). It works by removing all the introns and splicing back together exons. For nuclear-encoded genes, splicing occurs in the nucleus either during or immediately after transcription. For those eukaryotic genes that contain introns, splicing is usually needed to create an mRNA molecule that can be translated into protein. For many eukaryotic introns, splicing occurs in a series of reactions which are catalyzed by the spliceosome, a complex of small nuclear ribonucleoproteins (snRNPs). There exist self-splicing introns, that is, ribozymes that can catalyze their own excision from their parent RNA molecule. The process of transcription, splicing and translation is called gene expression, the central dogma of molecular biology.

<span class="mw-page-title-main">Alternative splicing</span> Process by which a gene can code for multiple proteins

Alternative splicing, or alternative RNA splicing, or differential splicing, is an alternative splicing process during gene expression that allows a single gene to produce different splice variants. For example, some exons of a gene may be included within or excluded from the final RNA product of the gene. This means the exons are joined in different combinations, leading to different splice variants. In the case of protein-coding genes, the proteins translated from these splice variants may contain differences in their amino acid sequence and in their biological functions.

Trans-splicing is a special form of RNA processing where exons from two different primary RNA transcripts are joined end to end and ligated. It is usually found in eukaryotes and mediated by the spliceosome, although some bacteria and archaea also have "half-genes" for tRNAs.

<span class="mw-page-title-main">DSCAM</span> Protein-coding gene in the species Homo sapiens

DSCAM and Dscam are both abbreviations for Down syndrome cell adhesion molecule. In humans, DSCAM refers to a gene that encodes one of several protein isoforms.

<span class="mw-page-title-main">PAX6</span> Protein-coding gene in humans

Paired box protein Pax-6, also known as aniridia type II protein (AN2) or oculorhombin, is a protein that in humans is encoded by the PAX6 gene.

Exon shuffling is a molecular mechanism for the formation of new genes. It is a process through which two or more exons from different genes can be brought together ectopically, or the same exon can be duplicated, to create a new exon-intron structure. There are different mechanisms through which exon shuffling occurs: transposon mediated exon shuffling, crossover during sexual recombination of parental genomes and illegitimate recombination.

<span class="mw-page-title-main">Group II intron</span> Class of self-catalyzing ribozymes

Group II introns are a large class of self-catalytic ribozymes and mobile genetic elements found within the genes of all three domains of life. Ribozyme activity can occur under high-salt conditions in vitro. However, assistance from proteins is required for in vivo splicing. In contrast to group I introns, intron excision occurs in the absence of GTP and involves the formation of a lariat, with an A-residue branchpoint strongly resembling that found in lariats formed during splicing of nuclear pre-mRNA. It is hypothesized that pre-mRNA splicing may have evolved from group II introns, due to the similar catalytic mechanism as well as the structural similarity of the Group II Domain V substructure to the U6/U2 extended snRNA. Finally, their ability to site-specifically insert into DNA sites has been exploited as a tool for biotechnology. For example, group II introns can be modified to make site-specific genome insertions and deliver cargo DNA such as reporter genes or lox sites

In molecular biology, an exonic splicing enhancer (ESE) is a DNA sequence motif consisting of 6 bases within an exon that directs, or enhances, accurate splicing of heterogeneous nuclear RNA (hnRNA) or pre-mRNA into messenger RNA (mRNA).

<span class="mw-page-title-main">Untranslated region</span> Non-coding regions on either end of mRNA

In molecular genetics, an untranslated region refers to either of two sections, one on each side of a coding sequence on a strand of mRNA. If it is found on the 5' side, it is called the 5' UTR, or if it is found on the 3' side, it is called the 3' UTR. mRNA is RNA that carries information from DNA to the ribosome, the site of protein synthesis (translation) within a cell. The mRNA is initially transcribed from the corresponding DNA sequence and then translated into protein. However, several regions of the mRNA are usually not translated into protein, including the 5' and 3' UTRs.

<span class="mw-page-title-main">TNNT1</span> Protein-coding gene in the species Homo sapiens

Slow skeletal muscle troponin T (sTnT) is a protein that in humans is encoded by the TNNT1 gene.

<span class="mw-page-title-main">RBP3</span> Protein-coding gene in the species Homo sapiens

Retinol-binding protein 3, interstitial (RBP3), also known as interphotoreceptor retinoid-binding protein (IRBP), is a protein that in humans is encoded by the RBP3 gene. RBP3 orthologs have been identified in most eutherians except tenrecs and armadillos. A horizontal gene transfer from bacteria has been proposed to explain the evolution of the eye in chordates.

<span class="mw-page-title-main">Genome evolution</span> Process by which a genome changes in structure or size over time

Genome evolution is the process by which a genome changes in structure (sequence) or size over time. The study of genome evolution involves multiple fields such as structural analysis of the genome, the study of genomic parasites, gene and ancient genome duplications, polyploidy, and comparative genomics. Genome evolution is a constantly changing and evolving field due to the steadily growing number of sequenced genomes, both prokaryotic and eukaryotic, available to the scientific community and the public at large.

Periannan Senapathy is a molecular biologist, geneticist, author and entrepreneur. He is the founder, president and chief scientific officer at Genome International Corporation, a biotechnology, bioinformatics, and information technology firm based in Madison, Wisconsin, which develops computational genomics applications of next-generation DNA sequencing (NGS) and clinical decision support systems for analyzing patient genome data that aids in diagnosis and treatment of diseases.

<span class="mw-page-title-main">SWAP protein domain</span>

In molecular biology, the protein domain SWAP is derived from the term Suppressor-of-White-APricot, a splicing regulator from the model organism Drosophila melanogaster. The protein domain is found in regulators that control splicing. It is found in splicing regulatory proteins. When a gene is expressed the DNA must be transcribed into messenger RNA (mRNA). However, it sometimes contains intervening or interrupting sequences named introns. mRNA splicing helps to remove these sequences, leaving a more favourable sequence. mRNA splicing is an essential event in the post-transcriptional modification process of gene expression. SWAP helps to control this process in all cells except gametes.

Exitrons are produced through alternative splicing and have characteristics of both introns and exons, but are described as retained introns. Even though they are considered introns, which are typically cut out of pre mRNA sequences, there are significant problems that arise when exitrons are spliced out of these strands, with the most obvious result being altered protein structures and functions. They were first discovered in plants, but have recently been found in metazoan species as well.

The split gene theory is a theory of the origin of introns, long non-coding sequences in eukaryotic genes between the exons. The theory holds that the randomness of primordial DNA sequences would only permit small (< 600bp) open reading frames (ORFs), and that important intron structures and regulatory sequences are derived from stop codons. In this introns-first framework, the spliceosomal machinery and the nucleus evolved due to the necessity to join these ORFs into larger proteins, and that intronless bacterial genes are less ancestral than the split eukaryotic genes. The theory originated with Periannan Senapathy.

An outron is a nucleotide sequence at the 5' end of the primary transcript of a gene that is removed by a special form of RNA splicing during maturation of the final RNA product. Whereas intron sequences are located inside the gene, outron sequences lie outside the gene.

Constructive neutral evolution(CNE) is a theory that seeks to explain how complex systems can evolve through neutral transitions and spread through a population by chance fixation (genetic drift). Constructive neutral evolution is a competitor for both adaptationist explanations for the emergence of complex traits and hypotheses positing that a complex trait emerged as a response to a deleterious development in an organism. Constructive neutral evolution often leads to irreversible or "irremediable" complexity and produces systems which, instead of being finely adapted for performing a task, represent an excess complexity that has been described with terms such as "runaway bureaucracy" or even a "Rube Goldberg machine".

References

  1. 1 2 3 4 Jacob, François (1977). "Evolution and Tinkering". Science. 196 (4295): 1161–1166. Bibcode:1977Sci...196.1161J. doi:10.1126/science.860134. ISSN   0036-8075. JSTOR   1744610. PMID   860134.
  2. ↑ Sanger, Mary Bryna; Levin, Martin A. (1992). "Using Old Stuff in New Ways: Innovation as a Case of Evolutionary Tinkering". Journal of Policy Analysis and Management. 11 (1): 88–115. doi:10.2307/3325134. ISSN   0276-8739. JSTOR   3325134.
  3. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 Graur, Dan (2016). "Chapter 8: Evolution by Molecular Tinkering". Molecular and Genome Evolution. Sunderland, MA: Sinauer Associates, Inc. pp. 339–390. ISBN   9781605354699.
  4. ↑ Morange, Michel (2013-05-23). "François Jacob (1920–2013)". Nature. 497 (7450): 440. Bibcode:2013Natur.497..440M. doi:10.1038/497440a. ISSN   0028-0836. PMID   23698437.
  5. ↑ Darwin, Charles (1900). Origin of species / Charles Darwin. New York, Boston: H.M. Caldwell Co. doi:10.5962/bhl.title.959.
  6. ↑ de Lorenzo, Víctor (December 2018). "Evolutionary tinkering vs. rational engineering in the times of synthetic biology". Life Sciences, Society and Policy. 14 (1): 18. doi: 10.1186/s40504-018-0086-x . ISSN   2195-7819. PMC   6087506 . PMID   30099657.
  7. ↑ Cupello, Camila; Hirasawa, Tatsuya; Tatsumi, Norifumi; Yabumoto, Yoshitaka; Gueriau, Pierre; Isogai, Sumio; Matsumoto, Ryoko; Saruwatari, Toshiro; King, Andrew; Hoshino, Masato; Uesugi, Kentaro; Okabe, Masataka; Brito, Paulo M (2022-07-26). Kuraku, Shigehiro; Bronner, Marianne E; Graham, Anthony; Long, John A (eds.). "Lung evolution in vertebrates and the water-to-land transition". eLife. 11: e77156. doi: 10.7554/eLife.77156 . ISSN   2050-084X. PMC   9323002 . PMID   35880746.
  8. ↑ MACLEAN, PAUL D. (November 1949). "Psychosomatic Disease and the "Visceral Brain"". Psychosomatic Medicine. 11 (6): 338–353. doi:10.1097/00006842-194911000-00003. ISSN   0033-3174. PMID   15410445.
  9. 1 2 Marks, John (December 2020). "François Jacob: Bricolage and the Possible". Nottingham French Studies. 59 (3): 333–349. doi:10.3366/nfs.2020.0294. ISSN   0029-4586.
  10. ↑ Grunberg-Manago, Marianne; Clark, Brian F. C.; Zachau, Hans G., eds. (1989). Evolutionary Tinkering in Gene Expression. doi:10.1007/978-1-4684-5664-6. ISBN   978-1-4684-5666-0.
  11. ↑ Graur, Dan (2016). "Chapter 7: Evolution by DNA Duplication". Molecular and Genome Evolution. Sunderland, MA: Sinauer Associates, Inc. pp. 273–338. ISBN   9781605354699.
  12. ↑ Kucej, Martin; Butow, Ronald A. (December 1, 2007). "Evolutionary tinkering with mitochondrial nucleoids". Trends in Cell Biology. 17 (12): 586–592. doi:10.1016/j.tcb.2007.08.007. PMID   17981466.
  13. ↑ Das, Sudeshna; Smith, Temple F (2000-01-01), "Identifying nature's protein lego set", Advances in Protein Chemistry, Analysis of Amino Acid Sequences, 54, Academic Press: 159–183, doi:10.1016/S0065-3233(00)54006-6, ISBN   978-0-12-034254-9, PMID   10829228 , retrieved 2024-05-08
  14. ↑ Koonin, Eugene V; Aravind, L; Kondrashov, Alexey S (June 9, 2000). "The Impact of Comparative Genomics on Our Understanding of Evolution". Cell. 101 (6): 573–576. doi: 10.1016/S0092-8674(00)80867-3 . PMID   10892642.
  15. ↑ Cohen-Gihon, Inbar; Sharan, Roded; Nussinov, Ruth (2011-06-01). "Processes of fungal proteome evolution and gain of function: gene duplication and domain rearrangement". Physical Biology. 8 (3): 035009. Bibcode:2011PhBio...8c5009C. doi:10.1088/1478-3975/8/3/035009. ISSN   1478-3975. PMC   3140765 . PMID   21572172.
  16. ↑ Letunic, I. (2002-06-15). "Common exon duplication in animals and its role in alternative splicing". Human Molecular Genetics. 11 (13): 1561–1567. doi:10.1093/hmg/11.13.1561. PMID   12045209.
  17. ↑ Kawashima, Takeshi; Kawashima, Shuichi; Tanaka, Chisaki; Murai, Miho; Yoneda, Masahiko; Putnam, Nicholas H.; Rokhsar, Daniel S.; Kanehisa, Minoru; Satoh, Nori; Wada, Hiroshi (May 14, 2009). "Domain shuffling and the evolution of vertebrates". Genome Research. 19 (8): 1393–1403. doi:10.1101/gr.087072.108. ISSN   1088-9051. PMC   2720177 . PMID   19443856.
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