Annual Plant Reviews Arthur Hunt Boeing 747 CCC chloroquine complexity cluster Cochliobolus heterostrophus Darwin Devolves Darwin's Black Box Darwin's Doubt devolution DNA Evolution Francoise Budar Fred Hoyle fungal pathogen gene hydrophilic molecules Irreducible Complexity John Jay College Latest Life Sciences maize male sterility Manyuan Long Michael Behe mitochondria Molecular Biology of the Cell Nathan Lents Panda's Thumb Parvez Sofi probabilistic resources protein Richard Berthome Southern corn leaf blight Stephen Meyer T-urf13 The Edge of Evolution University of Kentucky URF13 Zea mays L

Is T-urf13 reversed by Irreducible Complexity? Reply Arthur Hunt

Reducing Complexity

Biologist Arthur Hunt is Professor of Plant and Soil Science on the University of Kentucky. Since 2007, he has claimed to have refused Michael Behe's claim that trivial complexity cannot be created by insane evolutionary processes. Particularly, he refers back to the instance he claims is an inextricably complicated system that arises from scratch. An example is a mitochondrial gene referred to as T-urf13, which encodes an ion-conducting channel referred to as URF13, which is restricted for maize mitochondria (maize plant Zea mays L). In January this yr, Hunt revealed an up to date article on the internet that you could entry and download here. And now Been's new ebook, Darwin Devolves, revealed in Skeptic Journal, biologist Nathan Lents at John Jay School, based mostly on an article by Hunt, confidently declares that T-urf13 is a “clear example of random tinkering exactly what [19459019

Hunt article begins :

Lately there has been interest within the blogosphere in protein evolution, and particularly the suggestion that a new protein perform can develop. The unique version of this essay was adopted by Longin et al. Briefly, the varied mechanisms discussed within the evaluation embrace mixing the exon, overlapping the gene, retroposition, recruiting sequences of shifting parts, lateral gene transfer, gene fusion, and de novo initiation. Of all these mechanisms, with the least attention being given, the final one – the de novo phenomenon of the new protein coding genes – was principally "scratch". Some examples are talked about (reminiscent of anti-freeze proteins or AFGPs), and long-term followers of ev / cre conversations recognize players. Nevertheless, what I might say is probably the most spectacular of such examples by Lengthy et al. Not to point out

Nature Critiques Genetics article Hunt mentions what Manyuan Lengthy and his colleagues have written in 2003 (Long et al., 2003) has already been mentioned here and repealed for a long time, in addition to in Stephen Meyer's 2013 Darwin doubt (Meyer, 2013).

Hunt Continues:

Right here, I describe an example of a gene encoding a new protein that opens its eyes to access to evolutionary processes. For readers to actually read – what we study – is a protein that isn’t just a "simple" binding protein, or one which has some new physicochemical properties (corresponding to AFGP), however somewhat a fenced ion channel. Particularly, a multimeric complicated which: 1. allows the ions to move by means of the membranes; 2. and binds the "trigger" that gets the gate open (which is in any other case "closed" mode). Recalling that Behe, in Darwin's Black Box, explicitly invokes the gated ion channel IC techniques, the next quantities being an instance of a multifunctional IC system de Novo.

Hunt promises nice guarantees however doesn't ship.

For readers who would really like a summarized summary of future key points, here is a temporary evaluation:

  1. It is extremely unlikely that T-urf13 rose to de Novo's false mutations. This in itself is prima facie value considering for various explanations.
  2. The T-urf13 evolution requirement is "just that story", and no "presentation" of the "textbook" was provided for its origin. [19659011T-urf13isanon-intrinsicmalignantpropertyofasinglepotentiallybeneficialorganismpossiblyconsistentwithBehenDarwinDevolves
  3. .

Here’s a abstract of Hunt's argument and a few of the important crucial analyzes


The cornerstone of Hunt's argument primarily considerations the T-urf13 gene, which, contrary to the proposed "edge" of evolution of Behe ​​& # 39; developed very rapidly from other genes that decided rRNA in addition to some non-coding DNA parts. The gene defines a transmembrane protein that helps to facilitate the passage of hydrophilic molecules when maize is opened over a mitochondrial membrane only when specific molecules bind outdoors (Dewey and Levings, 1986). Protein is restricted for corn mitochondria with male sterile cytoplasm in Texas and can also be involved in causing male sterility and sensitivity to T-cytoplasm-specific fungal illnesses (Dewey et al., 1987; Hanson, 1991; Hack et al., 1991)

The protein was originally recognized in the mitochondrial genome of maize varieties grown for male sterility. T-urf13 has been discovered to be present solely in male-sterile T-cytoplasm (cmsT) maize. Between 1969 and 1970, the fields of cmsT maize have been destroyed because of the Cochliobolus heterostrophus fungal pathogen. This fungal pathogen produces a toxin that prompted a disease often known as Southern corn leaf blight in cmsT maize (Levings, 1990; Turgeon and Baker, 2007). The research revealed that both susceptibility to the illness and male sterility correlated with the presence of a new cmsT-specific locus encoding T-urf13. Hunt argues that this exhibits that Darwin has developed a gene. Hunt additional argues that T-urf13 is an irreducibly difficult system exactly the identical approach as Behe ​​claimed SRP-mediated transport to Darwin's Black Field. Identical to SRP-mediated transport requires a signal peptide, SRP and protein channel, T-urf13 consists of a fungus, a toxin-binding website and an ion channel. As Nathan Lents suggests, "that this structure was formed through several occasional DNA rearrangements, there is nothing incredible, but it is."

A number of points ought to be stored in mind as they problem this dissertation.

T-urf13 is unlikely to have awakened to De Novo at random

As has been stated, Hunt has prompt that T-urf13 rose from “de Novo” and “from scratch.” What exactly would this require for mutations? Within the unique publish of Hunt since 2007 on Pandan Thumb blog, he wrote

The underside line – T-urf13 consists of at the least three "CCCs". Some numbers make it potential to estimate that T-urf13 needs about 10 ^ 60 some sort of occasion for the occasion.

Readers can keep in mind the idea of "chloroquine complex cluster" (CCC) introduced in one other ebook by Michael Bee, The Fringe of Evolution (Behe, 2007). Behe found that the resistance of the antimalarial drug to chloroquine is rare and occurs solely once in 1020 cells of each of the cells of Plasmodium falciparum. Behe claimed that chloroquine resistance requires a minimum of two simultaneous level mutations. Considering empirical findings, this property is predicted to happen solely as soon as in 1020 organisms (White, 2004). In the case of Plasmodium falciparum, a malarial parasite, the organism has a adequate quantity to supply it. Nevertheless, there are not any different organisms like humans. Eukaryotes, similar to corn with crops, would definitely have far fewer organisms than single-cell parasites, which complicates the development of complicated options. Based on Bee, this barrier to chance is a serious problem to the idea of evolution

Arthur Hunt claims that there are at the very least three "CCCs" associated with the origin of T-urf13. He states

T-urf13 types in heteromeric complexes within the membrane. Which means at the very least two different subunits are sure by totally different subunits. Which means each subunit should have at the very least two totally different protein binding websites. It's at the very least two “CCCs…” Yet one more factor – the ion channel is fenced. It binds polycetide toxin and leads to the opening of the channel. That is the third binding website. This isn’t one other protein binding point, and I assume that Behe ​​would argue that this isn’t related to Evolution of Evolution. However the idea of "CCC" is predicated on Transporter (PfCRT) modifications that alter the interaction with chloroquine; the binding of the toxin to T-urf13 is sort of analogous to the interplay between PfCRT and chloroquine. The third perform of T-urf13 is thus just like the second "CCC".

Because of this Hunt points out that it’s anticipated to happen when Behe ​​only evaluates 1060 organisms as soon as. Because such an unbelievable function advanced, says Hunt, this means that the emergence of such options shouldn’t be, in any case, so sudden.

Hunt argues:

All this house message is: elements of the mitochondria of the corn genome that doesn’t usually encode any protein have been combined extensively in order to mix a gene encoding, not simply any previous polypeptide, but multimeter gated ion channel. In other words, one stroke resulted in an irreducibly complicated construction using DNA sequences that don’t encode proteins. Principally, that is an IC case from scratch.

But how does Hunt know that T-urf13 advanced with underexposed mutation occasions? He doesn’t. Or at the least he has not shown that T-urf13 would develop with blind improvement. Such a mixture of events, borrowing the words of Hunt, "one jump" seems actually unlikely by probability. That is particularly the case when it’s estimated that only 1040 organisms have lived within the life history of the whole nation (see Evolution of Evolution, p. 62). That is too little with factor 1020 for T-urf13 for de Novo improvement. And, in fact, if we think about the variety of eukaryotes or corn individuals, the magnitude of many will considerably scale back the number of experiments out there to supply a posh property corresponding to T-urf13. In truth, such a robust improbability should certainly, at first sight, lead us to think about the choice explanations offered by Hunt, specifically that the T-urf13 ion-combined channel was born by probability "with a single shot." chance assets, that it’s in itself a proof towards the potential for hypothesis, and will drive us to explore different attainable options.

“Just So” story for the originals of T-urf13

Neo-Darwin laughs at the critics of evolution who examine the theoretical evolutionary course of to the twister, which consists of the Boeing 747, initially an analogy by Fred Hoyle. Defenders of the Neo-Darwinian principle point out that evolution is just not a totally random course of, and that what can be extremely unlikely to be "one shot" might be damaged up into quite a few small, more doubtless levels, each of which provides some selective advantage that may be favored by a non-random pure choice. This is exactly what Richard Dawkins's guide Climbing Mount is unlikely. Although the unlikely entrance of the Mount is a rock that can’t be scaled by one massive leap, the back aspect has a regularly sloping path leading as much as the summit (Dawkins, 1996). Nevertheless, Hunt doesn’t depend on a phased evolutionary system through which each step has a chance of chance. Quite, the unlikely collection of occasions that Hunt invokes to elucidate the origin of this film-coated channel from "scratch" brings to mind a twister picture of a junkyard.

Although the T-urf13 gene has homology, different elements of the mitochondrial genome that don’t usually encode proteins are usually not adequate to type an evolutionary pathway. It hardly seems applicable to rely on mere sequence similarity to justify believing in extremely unlikely complicated rearrangements of DNA sequences with out first making any evaluation of the probability of such a state of affairs

One paper describing how T-urf13 is believed to have been born (Sofi et al., 2007 ), takes an strategy just like Hunt:

Turf 13 is a chimeric region gene that may be a recombination product of the 5 gene of & lt; 5 & gt; ribosomal gene (rrn 26). Its transcription is presumably beneath management of the lep 6 promoter (Stamper et al., 1987). It’s situated within the 3547 nucleotide mt DNA sequence containing two open reading frames, one encoding urf 13 and the other orf 221 encoding a 25 kd polypeptide consisting of 221 amino acids and 77 nucleotides urf 13: n downstream (Levings, 1990). Orf 221 encodes a membrane-bound protein identified as ATP4 (Heazlewood et al., 2003).

Observe that there are a minimum of five separate evolutionary events that must occur in order for T-urf13 to be generated: The primary two DNA fragments (lep 6 gene region 5 and the 265 ribosomal gene 3 & # 39; must be brought together utilizing a random mutation. Nevertheless, this alone is just not sufficient to supply a useful gene. The second step is to convey the lep 6 promoter to place for gene management. Third, Fourth, and Fifth: The three binding websites required for T-urf13 to perform must develop (two bind to subunits and the other bind to polycetocoxin that opens the gated channel). Presumably, until all these events occur, T-urf13 can’t work to offer any selectable advantage in sure contexts. Thus, Hunt's declare that it have to be "out of nothing". But what is the chance of all these occasions? No ID critic and any evolutionary biologist seems to care sufficient concerning the query.

There was no try in Arthur Hunt or T-urf13 literature to exhibit the probability of such a posh recombination occasion. If T-urf13 developed from scratch, the chance of its unimaginable origin has not been established.

T-urf13 is a malicious function

Another level value noting is that the phenotype is actually dangerous and not useful to the organism. It results in both male sterility and sensitivity to the fungus. T-urf13 is unlikely to survive in a pure setting and will only survive because it has been artificially chosen for people who need to develop corn sticks with maleism. The truth is, probably the most necessary reasons we all know that T-urf13 is liable for cytoplasmic male sterility and the sensitivity of the disease is the presence of revertant mutations that take away the T-urf13 gene in cell culture experiments, the place cms-T maize is grown with medium containing the BmT toxin, which makes the plant disease-resistant, and male fertile. Nevertheless, it’s shocking that when these experiments have been repeated with out toxin choice, random revertant mutations have been, nevertheless, obtained. These outcomes recommend that the T-urf13 gene offers a selective drawback unbiased of the sensitivity to BmT toxin (Pring et al., 1988).

The restriction enzyme mapping and nucleotide sequencing of mitochondrial DNA has been used to research a few dozen revertants, i.e. instances where T-urf13 was misplaced. Normally, the T-urf13 gene has been faraway from the mitochondrial genome because of recombination (Rottmann et al., 1987; Sensible et al., 1987; Fauron et al., 1990)

. it’s assumed that T-urf13 causes male sterility, that T-urf13 leads to a reduction in the effectiveness of mitochondrial exercise and that this causes the lack of crops to succeed in the edge of ATP production, which is indispensable for pollen improvement (Levings, 1993). Word that this can be a lack of perform. In truth, as Francoise Budar and Richard Berthome write within the chapter, they contributed to annual plant assessments, plant mitochondria (Budar and Berthome, 2007):

Evidence that mitochondrial exercise plays an essential position in plant progress is strongly supported. Lack of performance of the CMS mechanism for hypothesis. A plant where pollen manufacturing diminishes from mitochondrial metabolic issues seems to make the search for different forms of mechanisms unnecessary.

Actually, it has been discovered that a nuclear encoded protein referred to as Rf2, aldehyde dehydrogenase, is necessary in restoring fertility in male-sterile cmsT maize (Cui et al., 1996)

As summarized in Parvez Sof and colleagues (Sofi et al., 2007) 2007 assessment doc:

Cui et al. (1996) first proposed a working speculation on the position of Rf2 as a nuclear energy plant in CMS-T in maize and recommended that Rf2 be restored to fertility by enhancing the mitochondria associated with the expression of the Turf 13 gene. Two routes complete this improvement. One is metabolism, whereby the power produced by the oxidation of ALDH fatty acids compensates for the potential power shortage of wallpaper. Alternatively, ALDH acts by detoxifying acetaldehyde. The interaction mode includes the interaction of ALDH and Urf-13, which reduces its dangerous effects. In reality, the shortage of ALDH exercise of mitochondria causes complete male sterility in T-cytoplasm (Liu et al., 2001). [Emphasis added.]

So it is quite clear that Arthur Hunt, Nathan Lents, and others as an elective instance of a brand new protein complicated which are born by de Novo, Arthur Hunt, Nathan Lents and others, need to promote a system that itself trigger harm to the organism. it carries it. Certainly if there was a greater instance – which is functionally useful to the organism – then they might as an alternative be touting. The statement in Hunt's essay is that his example "should open his eyes to the processes of evolution." And as soon as once more, his example proves to be one that damages and does not benefit the organism. It’s also curious that Hunt's evolution mannequin requires an unimaginable collection of mutations that attach to the corn strain, however not with the intention of gaining advantages for the organism! There seems to be something else right here.

Origins of T-urf13 In all probability associated with lack of perform

If T-urf13 is usually dangerous and continues mainly as a result of man's artificial selection, how was it born? Everybody agrees that it was born by probability. However did it awaken to de Novo or does it characterize the decomposition of any previous gene? As an alternative of T-urf13 being "one shot", it is extra probably that its origin is accompanied by a loss of functionality, equivalent to what Behe ​​writes in Darwin Devolves and earlier in Evolution of Evolution (Behe, 2007; Behe, 2019).

As famous, T-urf13, which is found solely in this maize subfamily, has similarity to URF-13, which happens extra extensively in native maize. One attainable state of affairs is that the URF-13 complicated is involved in another course of and that it was damaged so that it was not properly regulated. The primary identification of T-urf13 preceded lengthy before the maize genome was sequenced in the early 2000s (Chandler and Brendel, 2002; Schnable et al., 2009; Soderlund et al., 2009; Gore et al., 2009 Vielle-Calzada et al. 2009). Thus, it was inconceivable to find out whether the T-urf13 gene really had "reappeared" or whether or not it was already present and did something else. Is there proof to help such a hypothesis? First, as already talked about, T-urf13 appears to be beneath the control of a nuclear encoded protein, specifically Rf2 (Cui et al., 1996). This seems to recommend that T-urf13 might have been previously concerned in different processes

The proteins embedded in the mitochondrial membrane are synthesized within the cytosol, and subsequently have an alpha-helical apipate coil at the N-terminus identified by the transport complexes (see this section on mobile molecular biology). . It follows that there ought to be a sign peptide for insertion of the mitochondrial membrane. Because of this what we’ve is, in truth, the insertion of DNA into an present gene that itself was a membrane protein for mitochondria and perhaps a channel – and maybe a regulated channel as a result of it affects it. The Signal-BLAST device on the website of the Middle for Utilized Molecular Know-how (CAME) allows the consumer to determine signal peptides within the protein sequence (Frank and Sippl, 2008). Getting into a FASTA file for T-urf13 produces a sign peptide outcome after the assumed cleavage website AA 35 (just like RLF32_ARATH). RLF32_ARATH is a signal peptide that imports the Arabidopsis gene into mitochondria. This protein is concerned in cellular cell signaling by way of the Ca ++ circulate. All because of this T-urf13 in all probability came from a totally useful, already present gene and was not born de Novo.

In abstract

Briefly, the very first thing to know about T-urf13 is that it is a malicious function. It’s related to the sensitivity to fungicide and in addition correlates with male sterility. It’s going to solely survive due to the man's selection of corn sticks, and it in all probability won’t remain in its personal nature.

One other factor to be understood from T-urf13 is that solely Texas corn is a sub-strain of corn that represents only a fraction of the whole number of particular person corn crops compared to the entire corn population. 19659003] Arthur Hunt's rationalization is accompanied by a collection of occasions that might require up to 1060 individuals to supply de Novo or "from scratch" by way of totally inevitable, probably evolving mutation processes. And this occurred in a small corn pressure, which DOES NOT need to produce a considerably advantageous property, however produces a dangerous property which then spread by means of the strain.

His story seems to be impossible at many levels. To begin with, there are considerably insufficient chance assets that produce a property in this corn sub-strain, much less in all wheat, a lot much less in all crops, a lot less in all crops which have lived within the historical past of the entire nation, a lot much less in all organisms that have lived within the history of the country. The proponents of conventional evolutionary principle typically say "Wow, isn't it amazing that this thing evolved!" However this can be a backward reasoning because they haven’t shown that it advanced. They ignore chance questions. If an individual works like a scientist and holds math, Hunt's unlikely evolutionary system is pretend. It appears that evidently wild speculation is just unlikely and must be ignored.

The third factor to know is that everybody agrees that T-urf13 was born by probability. However by probability, it doesn’t imply that it was purported to be from scratch. As Michael Behe ​​has explained, random mutations, which are not neutral, usually break issues on the molecular degree. Arthur Hunt doesn't like this chance and claims it was born out of nothing. Nevertheless, taking arithmetic and information under consideration leads to a unique rationalization. And since Hunt's "one jump" is nothing more than speculation, we are allowed to recommend our own model, albeit a bit speculative. Listed here are three key details to think about:

  • The high chance of creating T-urf13 de Novo from scratch is in itself an argument towards such a hypothesis.
  • Random mutations break or uninteresting molecular features far more typically than they create new ones.
  • T-urf13 is subject to nuclear regulation that is in step with its earlier involvement in other processes

These information might result in ID-inspired Behe-esque-spreading hypotheses which might be in step with recognized evidence: The URF13 mitochondrial channel, which correlates with the cytoplasmic male sterility and sensitivity to the fungicide, truly advanced from the gates on a channel that performs a number of the corn activity regulated by regulation. On this state of affairs, URF13 developed – NOT "scratch", although. As an alternative, it moved from an present protein that was once absolutely practical, but whose regulation was damaged. Nevertheless, the ensuing broken property is harmful to the organism and is associated with male sterility and fungicides. Thus, there are numerous twists and turns that merely take away T-urf13 and eliminate the issues it causes.

This is certainly a speculative state of affairs (in this respect there isn’t a difference from the Hunt). However it has clear benefits over Hunt's rationalization:

  1. It isn’t unreasonably unlikely, and it does not rely on a impossible collection of mutations that would never be born in small populations, comparable to this corn subpopulation
  2. t depend on a wildly unlikely evolutionary system to do one thing that Lastly, not even help the organism.
  3. It takes under consideration that random mutations are likely to disrupt or uninteresting molecular features rather more typically than new ones.
  4. It explains why T-urf13 is regulated by mycene.

Further research may help check these hypotheses; The origin of T-urf13 is an fascinating query that deserves additional research. At present, one model that has not likely been proven is Arthur Hunt's suggestion that T-urf13 advanced from "de Novo" and "from scratch".

Literature Talked about

  • Behe, MJ (2019) Darwin Devolves: The New Science About DNA that challenges evolution. HarperOne
  • Behe, M.J. (2007) Evolution: Finding the boundaries of Darwinism.
  • Budar, F. and Berthome, R. (2007) Cytoplasmic Male Sterilities and Mitochondrial Gene Mutations in Crops. In the ebook Annual Plant Evaluate Volume 31: Plant Mitochondria.
  • Chandler, V.L. and Brendel, V. (2002) Maize Genome Sequencing Challenge. Plant Physiology 130: 1594-1597
  • Cui, X., Clever, R.P. and Schnable, P.S. (1996) RF2 Nuclear Repairer gene for male sterile T-cytoplasm. Science 272: 1334-1336.
  • Dawkins, R. (1996) Climbing frame unlikely. Penguin.
  • Dewey, R.E. and Levings, C.S. (1986) New recombinations within the maize mitochondrial genome produce a singular transcription unit within the male sterile cytoplasm of Texas. Cell 44 (3): 439-449.
  • Dewey, R.E., Timothy, D.H., Levings, C.S. (1987) mitochondrial protein related to cytoplasmic male sterility in maize T-cytoplasm. National Academy of Sciences Publication US 48 (15): 5374-5378.
  • Fauron, C. M.R., Havlik, M., and Brettell, R.I.S. (1990) The genomic arrangement of mitochondria within the fertile cmsT revertant line of maize is generated by recombination between two repeat techniques. Genetics 124, 423-428.
  • Frank, Okay. and Manfred, J. (2008) Sippl High Efficiency Sign Peptide Prediction Based mostly on Sequence Concentrating on Methods. Bioinformatics 24: 2172-2176
  • Gore, M.A. et al. The first era of haplotype corn. Science 326 (5956): 1115-1117.
  • Hack, E., Lin, C., Yang, H. and Horner, H.T. (1991) T-URF 13 protein from mitochondria of male sterile maize (Zea mays L.) in Texas. Plant Physiology 95 (3): 861-870.
  • Hanson, M.R. (1991) Plant mitochondrial mutations and male sterility. Genetics Annual Evaluation 25: 461-86.
  • Keefe, A.D. and Szostak, J.W. (2001) Useful proteins from a random sequence library. Nature 410: 715-718.
  • Levings, C.S. (1990) Texas cytoplasm in corn: cytoplasmic male sterility and disease sensitivity. Science 250: 942-947.
  • Levings, C.S. (1993) thoughts of cytoplasmic male sterile in cms-T maize. The Plant Cell 5: 1285-1290.
  • Lengthy, M., Betran, E., Thornton, Okay., and Wang, W. (2003) Origin of New Genes: Blinking from Young and Previous. Nature Critiques Genetics 4: 865-875.
  • Meyer, S. C. (2013) Darwin's doubt: the explosive origin of animal life and intelligent design. HarperOne.
  • Pring, D.R., Gengenbach, B.G. and Sensible, R.P. (1988). Recombination is related to polymorphism of mitochondrial genomes in corn and sorghum. Royal Society B 319: 187-198 Philosophical Transactions
  • Rottmann, W.H., Brears, T., Hodge, T.P. and Lonsdale, D.M. (1987). The mitochondrial gene is lost by homologous recombination in the course of the recovery of CMS T to fertility. EMBO Journal 6: 1541-1546
  • Schnable, P.S. et al. (2009) B73 genome: complexity, variety and dynamics. Science 326 (5956): 1112-1115.
  • Soderlund et al. (2009) 27,455 sequencing, mapping and analysis of full-length corn cDNA. PLoS Genetics 5 (11): e1000740.
  • Sofi, P.A., Slightly, A.G. and Wani, S.A. (2007) Genetic and molecular basis of cytoplasmic male sterility in maize. Viestintä biometriassa ja Crop Science 2: ssa (1): 49-60.
  • Turgeon, B.G. ja Baker, S.E. (2007) Cochliobolus heterostrophus Tox1 -paikan geneettinen ja genominen dissektio, joka kontrolloi polyketidivirulenssitekijän T-toksiinin biosynteesiä. Advances in Genetics 57: 219-261.
  • Vielle-Calzada et ai. (2009) Palomero-genomi ehdottaa metallien vaikutuksia kotitykseen. Science 326 (5956): 1078.
  • White, N.J. The Journal of Medical Investigation 113 (eight): 1084 – 1092.
  • Sensible, R.P., Pring, D. R. ja Gengenbach, B.G. (1987). Mutaatio miehen hedelmällisyyteen ja toksiinin epäherkkyyteen Texas (T) -sytoplasman maississa liittyy kehysmuutokseen mitokondrioiden avoimeen lukukehykseen. Kansallisen tiedeakatemian julkaisut USA 84: 2858-2862.

Valokuvaluotto: A cornfield, Freestyle nl [CC BY-SA 3.0]Wikimedia Commonsin kautta

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