O DNA mitocondrial é inadequado para testar o isolamento por distância

sexta-feira, dezembro 14, 2018

Mitochondrial DNA is unsuitable to test for isolation by distance

Peter R. Teske, Tirupathi Rao Golla, Jonathan Sandoval-Castillo, Arsalan Emami-Khoyi, Carl D. van der Lingen, Sophie von der Heyden, Brent Chiazzari, Bettine Jansen van Vuuren & Luciano B. Beheregaray 

Scientific Reports volume 8, Article number: 8448 (2018) 


Abstract

Tests for isolation by distance (IBD) are the most commonly used method of assessing spatial genetic structure. Many studies have exclusively used mitochondrial DNA (mtDNA) sequences to test for IBD, but this marker is often in conflict with multilocus markers. Here, we report a review of the literature on IBD, with the aims of determining (a) whether significant IBD is primarily a result of lumping spatially discrete populations, and (b) whether microsatellite datasets are more likely to detect IBD when mtDNA does not. We also provide empirical data from four species in which mtDNA failed to detect IBD by comparing these with microsatellite and SNP data. Our results confirm that IBD is mostly found when distinct regional populations are pooled, and this trend disappears when each is analysed separately. Discrepancies between markers were found in almost half of the studies reviewed, and microsatellites were more likely to detect IBD when mtDNA did not. Our empirical data rejected the lack of IBD in the four species studied, and support for IBD was particularly strong for the SNP data. We conclude that mtDNA sequence data are often not suitable to test for IBD, and can be misleading about species’ true dispersal potential. The observed failure of mtDNA to reliably detect IBD, in addition to being a single-locus marker, is likely a result of a selection-driven reduction in genetic diversity obscuring spatial genetic differentiation.

Acknowledgements

This study was funded by the National Research Foundation (CSUR Grant No. 87702 to P.R.T.), the University of Johannesburg (URC/FRC grant to P.R.T) and the Australian Research Council (FT130101068 and DP110101275 to L.B.B.). T.R.G. and A.E.-K. acknowledge the University of Johannesburg for Global Excellence and Stature (GES) fellowships for doctoral and postdoctoral study, respectively. We are grateful to two anonymous reviewers whose comments improved the quality of this manuscript.

Author information

Author notes

Peter R. Teske and Tirupathi Rao Golla contributed equally to this work.

Affiliations

Centre for Ecological Genomics and Wildlife Conservation, Department of Zoology, University of Johannesburg, Auckland Park, 2006, South Africa

Peter R. Teske, Tirupathi Rao Golla, Arsalan Emami-Khoyi & Bettine Jansen van Vuuren

Molecular Ecology Lab, College of Science and Engineering, Flinders University, Adelaide, SA, 5001, Australia

Jonathan Sandoval-Castillo & Luciano B. Beheregaray

Branch: Fisheries Management, Department of Agriculture, Forestry and Fisheries, Private Bag X2, Vlaeberg, 8012, South Africa

Carl D. van der Lingen

Department of Biological Sciences and Marine Research Institute, University of Cape Town, Private Bag X3, Rondebosch, 7700, South Africa

Carl D. van der Lingen

Evolutionary Genomics Group, Department of Botany and Zoology, University of Stellenbosch, Private Bag X1, 7602, Matieland, South Africa

Sophie von der Heyden

School of Life Sciences, University of KwaZulu-Natal, Westville, Durban, 4001, South Africa

Brent Chiazzari

Contributions

P.R.T. and L.B.B. designed the study; C.v.d.L., P.R.T., S.v.d.H., B.C. and J.S.-C. collected the samples; P.R.T. and T.R.G. conducted the literature review; P.R.T., J.S.-C., T.R.G. and A.E.-K. analysed the data; P.R.T., L.B.B., T.R.G. and S.v.d.H. wrote the paper, with input from C.v.d.L., J.S.-C., B.v.V. and B.C.

Competing Interests

The authors declare no competing interests.

Corresponding author

Correspondence to Peter R. Teske.

FREE PDF GRATIS: Scientific Reports Sup. Info.

Relatório anual de Inteligência Artificial 2018

quinta-feira, dezembro 13, 2018

A "reincarnação" explica o transgenerismo???

Childhood Gender Nonconformity and Children’s Past-Life Memories

Marieta Pehlivanova, Monica J. Janke, Jack Lee & Jim B. Tucker

Received 30 May 2018, Accepted 04 Sep 2018, Published online: 15 Nov 2018



Abstract

Objectives: This study examines childhood gender nonconformity (GNC) in conjunction with the phenomenon in which young children describe memories of a purported previous life. Methods: In a case-control study of 469 children reporting past-life memories, we used logistic regression to examine predictors of GNC, measured by documented gender nonconforming behaviors. Results: Children who remembered a life involving a different natal sex were much more likely to exhibit GNC than children who remembered a same-sex life. Conclusions: After exploring potential explanations, we conclude that past-life memories represent a novel factor that may be associated with the development of GNC.

Keywords: Gender nonconformity, gender identity, children, adolescents, reincarnation memories

Subscription or payment needed/Requer assinatura ou pagamento:

International Journal of Sexual Health

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NOTA DESTE BLOGGER:

Essencialmente os pesquisadores estão dizendo que as experiências de "vidas passadas" relatadas por seus sujeitos de pesquisa (crianças) indicam a reencarnação. Isso levanta a questão do que, exatamente, está sendo reencarnado? Uma alma? Um espírito? Uma mente? Seja lá o que for, tem de ser imaterial. Mas isso vai de encontro ao que os biólogos evolucionistas vêm nos dizendo sobre o estado do universo e da biologia há décadas. Simplesmente não pode haver algo imaterial.  

O status científico desta pesquisa está na balança! Razão? Os pesquisadores são da Escola de Medicina da Universidade da Virgínia, Estados Unidos… não exatamente de uma universidade qualquer. E a publicação científica é uma das mais  prestigiadas na área de sexualidade humana.  

Este blogger queria ver a reação dos biólogos evolucionistas...

A química prebiótica e a intervenção humana: Maradona que o diga!

quarta-feira, dezembro 12, 2018

Prebiotic chemistry and human intervention

Clemens Richert 

Nature Communications volume 9, Article number: 5177 (2018) | Download Citation


Abstract

Experimentalists in the field of prebiotic chemistry strive to re-enact what may have happened when life arose from inanimate material. How often human intervention was needed to obtain a specific result in their studies is worth reporting.

Introduction

When Diego Maradona was asked about having used his hand to score a goal in the quarter-finals of the 1986 soccer World Cup, he initially claimed that there had been divine intervention, and the term “Hand of God Goal” was coined.—There had been manual intervention, and there had been an understandable interest of the player not to admit it.—Organic chemists, if not all experimentalists in the field of prebiotic chemistry, are faced with a similar dilemma. We do our best to perform experiments that we believe re-enact possible steps of prebiotic evolution, but we know that we need to intervene manually to obtain meaningful results. Simply mixing chemicals and watching for a living system to appear from the broth seems unreasonable to me. This approach has never worked, and it is not expected to work, at least not if one is limited to the lifetime of a human, let alone the duration of a funding period or a Ph.D. thesis. So, what is a reasonable level of intervention by the experimentalist in prebiotic chemistry, and what are “plausible prebiotic conditions” in this context?
...

FREE PDF GRATIS: Nature Communications

O que diferencia os primatas de outros mamíferos? Somente um gene?

segunda-feira, dezembro 10, 2018

A Primate-Specific Isoform of PLEKHG6 Regulates Neurogenesis and Neuronal Migration

Adam C. O’Neill Christina Kyrousi Johannes Klaus Richard J. Leventer Edwin P. Kirk Andrew Fry Daniela T. Pilz Tim Morgan Zandra A. Jenkins Micha Drukker  Samuel F. Berkovic Ingrid E. Scheffer Renzo Guerrini David M. Markie Magdalena Götz Silvia Cappello 16, 17 Stephen P. Robertson 16

Open AccessPublished: December 4, 2018  


Graphical Abstract:

Figure thumbnail fx1

Highlights

• Excess variants within basal radial glia transcriptomic signatures in cases of PH

• PLEKHG6 primate-specific isoform mutated in a case of PH functions via RhoA

• PLEKHG6 isoforms regulate features of neurogenesis

• Modulation of the PLEKHG6 primate isoform reproduces features of PH in organoids

Summary

The mammalian neocortex has undergone remarkable changes through evolution. A consequence of such rapid evolutionary events could be a trade-off that has rendered the brain susceptible to certain neurodevelopmental and neuropsychiatric conditions. We analyzed the exomes of 65 patients with the structural brain malformation periventricular nodular heterotopia (PH). De novo coding variants were observed in excess in genes defining a transcriptomic signature of basal radial glia, a cell type linked to brain evolution. In addition, we located two variants in human isoforms of two genes that have no ortholog in mice. Modulating the levels of one of these isoforms for the gene PLEKHG6 demonstrated its role in regulating neuroprogenitor differentiation and neuronal migration via RhoA, with phenotypic recapitulation of PH in human cerebral organoids. This suggests that this PLEKHG6 isoform is an example of a primate-specific genomic element supporting brain development.

FREE PDF GRATIS: Cell Reports

O cérebro no piloto automático: mero acaso, fortuita necessidade ou design inteligente?

Brain on Autopilot

How the architecture of the brain shapes its functioning.

By Max Planck Institute for Human Development

Lead image: Default Mode Network Credit: © Max Planck Institute for Human Development

The structure of the human brain is complex, reminiscent of a circuit diagram with countless connections. But what role does this architecture play in the functioning of the brain? To answer this question, researchers at the Max Planck Institute for Human Development in Berlin, in cooperation with colleagues at the Free University of Berlin and University Hospital Freiburg, have for the first time analyzed 1.6 billion connections within the brain simultaneously. They found the highest agreement between structure and information flow in the “default mode network,” which is responsible for inward-focused thinking such as daydreaming.

Everybody’s been there: You’re sitting at your desk, staring out the window, your thoughts wandering. Instead of getting on with what you’re supposed to be doing, you start mentally planning your next holiday or find yourself lost in a thought or a memory. It’s only later that you realize what has happened: Your brain has simply “changed channels”—and switched to autopilot.

For some time now, experts have been interested in the competition among different networks of the brain, which are able to suppress one another’s activity. If one of these approximately 20 networks is active, the others remain more or less silent. So if you’re thinking about your next holiday, it is almost impossible to follow the content of a text at the same time.

To find out how the anatomical structure of the brain impacts its functional networks, a team of researchers at the Max Planck Institute for Human Development in Berlin, in cooperation with colleagues at the Free University of Berlin and the University Hospital Freiburg, have analyzed the connections between a total of 40,000 tiny areas of the brain. Using functional magnetic resonance imaging, they examined a total of 1.6 billion possible anatomical connections between these different regions in 19 participants aged between 21 and 31 years. The research team compared these connections with the brain signals actually generated by the nerve cells.

Their results showed the highest agreement between brain structure and brain function in areas forming part of the “default mode network,” which is associated with daydreaming, imagination, and self-referential thought. “In comparison to other networks, the default mode network uses the most direct anatomical connections. We think that neuronal activity is automatically directed to level off at this network whenever there are no external influences on the brain,” says Andreas Horn, lead author of the study and researcher in the Center for Adaptive Rationality at the Max Planck Institute for Human Development in Berlin.

Living up to its name, the default mode network seems to become active in the absence of external influences. In other words, the anatomical structure of the brain seems to have a built-in autopilot setting. It should not, however, be confused with an idle state. On the contrary, daydreaming, imagination, and self-referential thought are complex tasks for the brain.

...

Read more here: Nautilus

Os acadêmicos são covardes? A força das pesquisas de queixas e os custos irrecuperáveis da carreira acadêmica

quarta-feira, dezembro 05, 2018

Are Academics Cowards? The Grip of Grievance Studies and the Sunk Costs of Academic Pursuit

Image result for cowardice
Source/Fonte: Times Higher Education

Posted on December 4, 2018 14 minute read by James A. Lindsay

There is much that should be said about the ways in which the dominant Social Justice ideology has negative impacts upon the university, free expression, academic freedom and, especially, the sciences. Like all rigid ideologies, Social Justice is inimical to science—not because of what it claims or concludes but because of how it goes about reaching its conclusions. Social Justice, like all rigid ideologies, is only interested in science that supports its predetermined theoretical conclusions and holds all other science suspect.

Of course, the accusation that the sciences are susceptible to the forces of Social Justice and its endless politicking may come as some surprise to those in the sciences, because they are duly confident in their own rigor. They are right to realize that, even if the Social Justice educational reformers go too far or have a frightening amount of institutional control, they cannot really influence science directly because they don’t do science. The assumption held by many, which is plausible, is that scientists will keep doing science according to rigorous scientific methodologies and needn’t worry much about the influence of politics from the more ideological sectors of the academy—including the administration.

This attitude is both laudable and quaintly naive. It is likely to underestimate the degree to which the sciences, like all disciplines, are susceptible to the influences and whims of a dominant orthodoxy. We should note that this exact concern is also what we hear from proponents of Social Justice when they attempt to encroach upon science—it’s perhaps the chorus of the siren song of feminist studies of science and technology to insist that the sciences are already biased and that their activism is a necessary corrective. These criticisms of science insist that science is already prejudiced towards the ideological assumptions of white, Western men and therefore needs to be made more inclusive. This argument, however, goes against the core and essential nature of science, which is universality. Whatever is true about the world should be discoverable by the same methods, regardless of who or what does the experiment.

Another core part of the scientific process is skepticism. This means that science, as a process, is already geared to minimize and correct for potential biases and errors, be they ideological or otherwise. Input into ways to do this more efficiently are always welcome, but Social Justice approaches do not seek to further improve the objectivity of science. Instead, they aim to introduce opposing biases, which they see as effectively counteracting existing ones. Far from being a novel or useful insight, however, concerns about the lack of objectivity on the part of any given observer or theoretician aren’t lost on any serious scientist or philosopher of science and haven’t been in decades (and appropriating Thomas Kuhn’s work here doesn’t work on the Social Justice side).

For these reasons, scientists should be deeply concerned with the possibility that people with strongly ideological and political motives, many of which are ambivalent at best and hostile at worst to the core values of scientific inquiry, might establish themselves as the body of working scientists and arbiters of what science can and should be done and for what reasons. Rigorous epistemology and a certain willingness to let the cards fall where they may and to have one’s ideas proven wrong will suffice.

The thing is, it is extremely likely that a majority of working scientists, at least outside of the social sciences, are keenly aware of the ways in which Social Justice can corrupt science, its conflict with the core values of science and science education, and its potential costs and implications. Nevertheless, it appears that they are letting it happen. Why would they do this?

There’s no real mystery in this question. Most of the scientists who see the writing on the wall and wish they could do something about it will eagerly tell you precisely why they don’t speak and act against the creeping woke hegemony they know will eventually corrupt their disciplines, possibly for generations. They’re afraid. They’re afraid they’ll be fired. They’re afraid they’ll be blacklisted from jobs, tenure and research funding opportunities. They’re afraid they’ll become thorns in the sides of the administration, especially the Grand Wizards of their institutions’ Offices of Diversity and Inclusion, and targets of the newly minted campus inquisition Bias Response Teams, and never have another peaceful day to get real work done. They’re afraid they’ll be done like Tim Hunt was done.

Outside of the academy, this attitude often gets them branded cowards. In fact, the insistence that academics are cowardly, and that’s how we got into this mess in the first place, is one that seems to have a worrying level of support lately. It’s probably true that significant numbers of academics are cowards. In the main, however, it is only true in the sense in which a person is a coward for knowing that the first few to speak out in a revolt against any hegemonic regime are going to be its first martyrs. Speaking game theoretically, she who speaks out first should always be somebody else.

On those grounds, it’s probably not correct to say that academics are cowards. We hear exhortations that they should have the courage to risk their positions by speaking out because they have options. They have PhDs for God’s sake—surely they can get another job somewhere. This is a popular myth, but the opposite is nearer to the truth. Getting a PhD often locks a person into very few options other than to toe whatever line is needed to stay in academia. If we’re going to solve many of the institutional problems facing the academic working environment, not least the creep of Social Justice ideology into these institutions, the reality of the PhD job market is going to have to be taken into account.

To understand and find a workable path forward, we need to empathize.

Imagine yourself as a relatively new PhD. Chances are that you have spent anywhere between the last three and twelve years dedicated to higher education, and you have been following a path of increasing difficulty, paired with increasingly specific and narrow focus. By definition, supposing your committee and institution were up to the task and you’re not a rather extreme outlier, you should be for about eighteen months the world’s foremost authority on some exceptionally narrow topic within a subfield of whatever field you tell people that you got your doctorate in. You’re going to be competent in other aspects of that field, of course, but it’s important to remember that you’ve spent at least the last two or three years of your program (or the entire program, depending on the country where you studied) going right to the bottom of some fairly deep rabbit hole.

Why did you do this? Passion. Love. Interest. Enthusiasm. To pursue the simple dream of doing something you genuinely love doing.

It’s virtually impossible to push yourself through a PhD program unless you truly love the subject you’re studying and want to devote your working life to researching it and teaching it—which means getting an academic job. And earning a PhD isn’t exactly a picnic. (When I did my master’s degree, my reaction was that it was a bit surprising how easy it was to earn compared to my expectations going into the program. When I finished my Ph.D., the only thing I could say was, “they don’t give those away!”) In nearly every case, it takes a great deal of dedication, interest and passion to earn a PhD, to say nothing of luck and talent.

The phrase grad student is misleading. It seems to many kind of like Easy Street. But many PhD students and postdocs work obscene hours—often in excess of eighty hours a week—to keep up with their educational, research and job duties, especially if they want to do well enough to score a tenure-track job later. They usually get summers off from coursework so that they can work even harder on their research, so there’s no real break there. They also usually do this out of passion and grit because there’s hardly any money in graduate assistantship stipends in the wide majority of fields.

And don’t get this wrong. This isn’t a poor PhD candidate story: it’s a tale of investment. A PhD program isn’t just school (or college); it is just another kind of apprenticeship like that any master tradesperson has to go through, except that it takes about a decade of insanely hard work to get through the first stage of it. To earn a PhD requires an enormous investment of time, energy, talent and resources. And what do you get in return (besides your degree and a set of wizard’s robes, complete with a hooded cape and a goofy hat)? (Note: You have to buy the robes and hat, and they’re expensive. Further, you’ll never wear them again unless you go into academia professionally.)

Pause to consider this. Chances are, if you’re looking for academic jobs, especially in the sciences, you’re coming off a postdoc or two, so you’ve literally spent the last decade or more in training for the job you hope to get. You’ve made incredible sacrifices for it. You’ve invested more into getting past the first hurdle of a future career than almost anyone else. Just imagine training at double full time, paid less than minimum wage, for a decade for a job and then being able to think it’s worth risking the career you’re working for to make a political point, even a really important or necessary one.

It’s not easy to call that cowardice when you see what it’s really about.
...

Read more here: Aero

No mundo RNA, a vida tem mais um ingrediente... Próximo!

Inosine, but none of the 8-oxo-purines, is a plausible component of a primordial version of RNA

Seohyun Chris Kim, Derek K. O’Flaherty, Lijun Zhou, Victor S. Lelyveld, and Jack W. Szostak

PNAS published ahead of print December 3, 2018 https://doi.org/10.1073/pnas.1814367115

Edited by Gerald F. Joyce, The Salk Institute, La Jolla, CA, and approved October 26, 2018 (received for review August 21, 2018)

An artist's rendition of early Earth's hostile environment

Significance

The RNA world hypothesis assumes the abiotic synthesis of nucleotides, as well as their participation in nonenzymatic RNA replication. Whereas prebiotic syntheses of the canonical purine nucleotides remain inefficient, a prebiotically plausible route to the 8-oxo-purines has been reported. Although these noncanonical purine nucleotides are known to engage in non-Watson–Crick pairing with their canonical purine counterparts, their behavior in nonenzymatic RNA copying has not been evaluated. Our study indicates that none of the 8-oxo-purines behaves as a suitable substrate for nonenzymatic RNA copying. However, inosine turns out to exhibit reasonable rates and fidelities in RNA copying reactions. We propose that inosine could have served as a surrogate for guanosine in the early emergence of life.



Abstract

The emergence of primordial RNA-based life would have required the abiotic synthesis of nucleotides, and their participation in nonenzymatic RNA replication. Although considerable progress has been made toward potentially prebiotic syntheses of the pyrimidine nucleotides (C and U) and their 2-thio variants, efficient routes to the canonical purine nucleotides (A and G) remain elusive. Reported syntheses are low yielding and generate a large number of undesired side products. Recently, a potentially prebiotic pathway to 8-oxo-adenosine and 8-oxo-inosine has been demonstrated, raising the question of the suitability of the 8-oxo-purines as substrates for prebiotic RNA replication. Here we show that the 8-oxo-purine nucleotides are poor substrates for nonenzymatic RNA primer extension, both as activated monomers and when present in the template strand; their presence at the end of a primer also strongly reduces the rate and fidelity of primer extension. To provide a proper comparison with 8-oxo-inosine, we also examined primer extension reactions with inosine, and found that inosine exhibits surprisingly rapid and accurate nonenzymatic RNA copying. We propose that inosine, which can be derived from adenosine by deamination, could have acted as a surrogate for G in the earliest stages of the emergence of life.

origin of life RNA replication primordial RNA

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Especulações sobre os genomas dos procariontes não possuírem genes com introns processados por spliceossomos

sábado, dezembro 01, 2018

Journal of Molecular Evolution

December 2018, Volume 86, Issue 9, pp 611–612 | Cite as

Why Prokaryotes Genomes Lack Genes with Introns Processed by Spliceosomes?

Authors and affiliations

Guillermo Lamolle1, Héctor Musto1


1.Laboratorio de Organización y Evolución del Genoma, Unidad Genómica EvolutivaFacultad de CienciasMontevideoUruguay

First Online: 31 October 2018


Abstract

Until 1977, we thought that eukaryotic genes were like those of prokaryotes, that is, continuous sequences beginning with an initiation codon (ATG), followed by an open reading frame, always multiple of three bases (codons), and the message (mRNA) stopped when a stop codon (TAA, TAG or TGA) was reached. This paradigm, which historically seemed completely logical, changed dramatically when two groups, leaded by Sharp and Roberts (Berget et al. 1977; Chow et al. 1977), discovered that (at least some) eukaryotic protein coding genes were interrupted by non-coding sequences and eliminated from the mature (translated) mRNA before translation. Then, Gilbert (1978) coined the concept of exons (regions of the coding DNA that remained in the mRNA) and introns (the regions that are eliminated from the mature mRNA, and therefore are not present in the encoded proteins).

Today, there are no doubts that this discovery was a revolution in genetics. It not only challenged our previous definition of what a “gene” is, but led to discoveries and concepts such as splicing (that is, how introns are eliminated and exons are put together to make the mature mRNA), alternative splicing (how different exons from the same “gene” can be combined to make different proteins), or to the great discovery that some RNAs, once transcribed, can eliminate by themselves introns, a mechanism known as autosplicing (see, for instance, Bass and Cech 1986; Cech and Bass 1986; Guerrier-Takada and Altman 1986). In turn, the discovery of autosplicing not only reinforced the idea of the “RNA world” (for a review see Lehman 2015) but eliminated, forever, the time unanimous idea that proteins were the only catalytic molecules.

Therefore, the presence of introns in the majority of eukaryotic genes has challenged most of our concepts about genes, their regulation, their evolution, what is an enzyme… and last, but not least, why there are only probably fewer than 20,000 genes in the human genome while a “simple” organism like Escherichia coli has only around 4000. In other words, introns and how they are eliminated from the mature mRNAs has changed our concepts about molecular biology and evolution.

But given what we have said in the above lines (which of course do not pretend to be a review about the subject), there is a problem that, in our opinion, deserves some attention. As known, prokaryotes display an enormous divergence and different metabolic routes and lifestyles and occupy all known environments. Then, why did they never develop introns processed by spliceosomes? In the next few lines we shall propose an explanation.

Of course, the simplest one is that given that in prokaryotes transcription and translation are coupled, such a system should be a disadvantage from an evolutionary point of view. Furthermore, introns should be present. But there is no evidence that this was the case. Until now, nothing new. But there is a point that, in our opinion, seems very important.

As is known, the modern spliceosome, in its simplest form, is a complex of not less than ten different proteins and several RNAs. Let us imagine that this complex, or one even simplest, evolved in a prokaryote. And for some reason, which might be due to combine different genes in new, longest ones, it became fixed (or the existence or primitive introns). It is difficult to imagine such scenario, but let assume that it indeed happened, for example, “putting together” different pieces of genes from the same operon. This could be an advantage, because different pieces from different mRNAs could combine to produce new proteins with different, but related, functions. There is no biological constraint that can prevent this. Even more, it should be a new way to create new genes and, as a consequence, new functions. We stress that this scenario is hard to imagine just because (as far as we know) it did not happen. But if there was an example, it should not be a big surprise.

However in our opinion it did not happen because of another reason: one of the main forces in the evolution of prokaryotes is horizontal gene transfer (see, for example, Puigbò et al. 2010). As is known, for a gene (or group of genes) to be fixed several biochemical and evolutionary “steps” must be fulfilled, among them are: (a) to be transferred as a unit, (b) to carry (or to be integrated near) a promoter, (c) to not disturb the normal functions of the receptor, and (d) to confer a selective advantage.

Very probably, a putative “primitive spliceosome” (PS) was not as complex as the modern one. But in any case, it should be a rather complex particle, composed by several proteins and RNAs. For it to be transferred successfully, several conditions are needed: (a) All the components of the PS should be transferred simultaneously, which is hard to imagine, because we need to postulate a large “PS operon”, which probably did not existed [sic] as such, and therefore, multiple events need to be invoked, which is very unlikely. (b) Introns cannot be possible in the receptor (otherwise, it should had a PS), and if they did not exist, a PS machinery very probably should be extremely harmful for the receptor and eliminated from the population, because of the non-adaptation of genes to the action of the xeno-PS. (c) Even if a and b were disregarded (which of course is more than unlikely), new genes acquired by HGT by the receptor of PS should be negatively affected by the PS acquired. Hence, new events of HGT should be eliminated by the receptor, eliminating, as a consequence, one the major forces in evolution.

Hence, we conclude that in the same manner that HGT was one of the main factors that contributed to fix the universal genetic code; as postulated by Vetsigian et al. (2006), it could be a major force inhibiting the appearance (and fixation) of introns processed by spliceosomes among prokaryotes.

Notes

Acknowledgements

Both authors are members of the Sistema Nacional de Investigadores, Uruguay.

Os efeitos da nicotina são transmitidos através das gerações de ratos: Lamarck redivivus???

sexta-feira, novembro 30, 2018

Nicotine exposure of male mice produces behavioral impairment in multiple generations of descendants

Deirdre M. McCarthy, Thomas J. Morgan Jr., Sarah E. Lowe, Matthew J. Williamson, Thomas J. Spencer, Joseph Biederman, Pradeep G. Bhide 


Source/Fonte: The Scientist

Abstract

Use of tobacco products is injurious to health in men and women. However, tobacco use by pregnant women receives greater scrutiny because it can also compromise the health of future generations. More men smoke cigarettes than women. Yet the impact of nicotine use by men upon their descendants has not been as widely scrutinized. We exposed male C57BL/6 mice to nicotine (200 μg/mL in drinking water) for 12 wk and bred the mice with drug-naïve females to produce the F1 generation. Male and female F1 mice were bred with drug-naïve partners to produce the F2 generation. We analyzed spontaneous locomotor activity, working memory, attention, and reversal learning in male and female F1 and F2 mice. Both male and female F1 mice derived from the nicotine-exposed males showed significant increases in spontaneous locomotor activity and significant deficits in reversal learning. The male F1 mice also showed significant deficits in attention, brain monoamine content, and dopamine receptor mRNA expression. Examination of the F2 generation showed that male F2 mice derived from paternally nicotine-exposed female F1 mice had significant deficits in reversal learning. Analysis of epigenetic changes in the spermatozoa of the nicotine-exposed male founders (F0) showed significant changes in global DNA methylation and DNA methylation at promoter regions of the dopamine D2 receptor gene. Our findings show that nicotine exposure of male mice produces behavioral changes in multiple generations of descendants. Nicotine-induced changes in spermatozoal DNA methylation are a plausible mechanism for the transgenerational transmission of the phenotypes. These findings underscore the need to enlarge the current focus of research and public policy targeting nicotine exposure of pregnant mothers by a more equitable focus on nicotine exposure of the mother and the father.

Author summary

Use of tobacco products is a major public health concern throughout the world. Cigarette smoking by pregnant women receives significant attention by scientific, public health, and public policy experts because it poses health risks for the mother and her children. Although more men smoke cigarettes than women, the health consequences of paternal smoking for their descendants are much less explored. Using a mouse model, we show that the offspring of nicotine-exposed males have hyperactivity, attention deficit, and cognitive inflexibility. These behavioral phenotypes are associated with attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder in humans. Cognitive inflexibility persists into the third (F2) generation. The neurotransmitters dopamine and noradrenaline and their receptors, critically implicated in neurodevelopmental disorders, are also altered in the offspring’s brains. The nicotine-exposed males show significant alterations in spermatozoal DNA methylation patterns, especially at dopamine receptor gene promoter regions, implicating epigenetic modification of germ cell DNA as a mechanism for the transgenerational transmission of the behavioral and neurotransmitter phenotypes. The impact of nicotine on germ cells and the neurobehavioral impairments in multiple subsequent generations call for renewed focus of research and public policy on tobacco use by men and its consequences for their descendants.

Citation: McCarthy DM, Morgan TJ Jr, Lowe SE, Williamson MJ, Spencer TJ, Biederman J, et al. (2018) Nicotine exposure of male mice produces behavioral impairment in multiple generations of descendants. PLoS Biol 16(10): e2006497. https://doi.org/10.1371/journal.pbio.2006497

Academic Editor: Eric Nestler, Icahn School of Medicine at Mount Sinai, United States of America

Received: April 27, 2018; Accepted: September 13, 2018; Published: October 16, 2018

Copyright: © 2018 McCarthy et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Data Availability: All relevant data are within the paper and its Supporting Information files.

Funding: Jim and Betty Anne Rodgers Chair Fund at Florida State University (grant number F00662). The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Escher Fund for Autism http://www.germlineexposures.org (grant number). The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. National Institute on Drug Abuse https://www.drugabuse.gov/ (grant number R15 DA043848). The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: I have read the journal's policy and the authors of this manuscript have the following potential competing interests. Pradeep Bhide: Dr. Bhide is a co-founder and consultant to Avekshan LLC, Tallahassee, FL, a pharmaceutical enterprise engaged in the development of novel therapies for attention deficit hyperactivity disorder (ADHD). Dr. Bhide is an inventor in following patents or patent applications relevant to ADHD therapy: US Patent, “Class of non-stimulant treatment and ADHD and related disorders” (#US9623023 B2), and US patent application, “Methods and compositions to prevent addiction (#US20130289061 A1). Deirdre McCarthy: Ms. McCarthy is a co-founder and consultant to Avekshan LLC, Tallahassee, FL, a pharmaceutical enterprise engaged in the development of novel therapies for attention deficit hyperactivity disorder (ADHD). Thomas Spencer: Dr. Spencer received research support or was a consultant from the following sources: Alcobra, Avekshan, Ironshore, Lundbeck, Shire Laboratories Inc, Sunovion, the FDA, and the Department of Defense. Consultant fees are paid to the Clinical Trials Network at the Massachusetts General Hospital (MGH) and not directly to Dr. Spencer. Dr. Spencer has been on an advisory board for the following pharmaceutical companies: Alcobra. Dr. Spencer received research support from Royalties and Licensing fees on copyrighted ADHD scales through MGH Corporate Sponsored Research and Licensing. Through MGH corporate licensing, Dr. Spencer is an inventor on a US Patent, “Class of non-stimulant treatment and ADHD and related disorders” (#US9623023 B2), and US patent application, “Methods and compositions to prevent addiction" (#US20130289061 A1). Joseph Biederman: Dr. Biederman is currently receiving research support from the following sources: AACAP, The Department of Defense, Food & Drug Administration, Headspace, Lundbeck, Neurocentria Inc., NIDA, PamLab, Pfizer, Shire Pharmaceuticals Inc., Sunovion, and NIH. Dr. Biederman has a financial interest in Avekshan LLC, a company that develops treatments for attention deficit hyperactivity disorder (ADHD). His interests were reviewed and are managed by Massachusetts General Hospital and Partners HealthCare in accordance with their conflict of interest policies. Dr. Biederman’s program has received departmental royalties from a copyrighted rating scale used for ADHD diagnoses, paid by Ingenix, Prophase, Shire, Bracket Global, Sunovion, and Theravance; these royalties were paid to the Department of Psychiatry at MGH. In 2017, Dr. Biederman is a consultant for Aevi Genomics, Akili, Guidepoint, Ironshore, Medgenics, and Piper Jaffray. He is on the scientific advisory board for Alcobra and Shire. He received honoraria from the MGH Psychiatry Academy for tuition-funded CME courses. Through MGH corporate licensing, he is an inventor on US Patent, “Class of non-stimulant treatment and ADHD and related disorders” (#US9623023 B2), and US patent application, “Methods and compositions to prevent addiction (#US20130289061 A1). In 2016, Dr. Biederman received honoraria from the MGH Psychiatry Academy for tuition-funded CME courses, and from Alcobra and APSARD. He was on the scientific advisory board for Arbor Pharmaceuticals. He was a consultant for Akili and Medgenics. He received research support from Merck and SPRITES. Thomas Morgan, Sara Lowe, and Matthew Williamson have no competing interests to declare.

Abbreviations: 3-MT, 3-methoxytyramine; ADHD, attention deficit hyperactivity disorder; DOPAC, 3,4-dihydroxyphenylacetic acid; HVA, homovanillic acid; MeDIP, methylated DNA immunoprecipitation; miRNA, microRNA; NE, norepinephrine; P0, postnatal day 0; qPCR, quantitative PCR

FREE PDF GRATIS: PLoS Biology

Princípios da geometria química subjacente à seletividade quiral na aminoacilação da mini hélice do RNA: mero acaso, fortuita necessidade ou design inteligente?

Principles of chemical geometry underlying chiral selectivity in RNA minihelix aminoacylation 

Tadashi Ando Shunichi Takahashi Koji Tamura

Nucleic Acids Research, Volume 46, Issue 21, 30 November 2018, Pages 11144–11152, https://doi.org/10.1093/nar/gky909

Published: 15 October 2018 

Article history

Received: 08 August 2018 Revision Received: 10 September 2018

Accepted: 02 October 2018

Image result for chemical geometry 
Source/Fonte: Courses Lumen Learning

Abstract

The origin of homochirality in L-amino acid in proteins is one of the mysteries of the evolution of life. Experimental studies show that a non-enzymatic aminoacylation reaction of an RNA minihelix has a preference for L-amino acid over D-amino acid. The reaction initiates by approaching of a 3′-oxygen of the RNA minihelix to the carbonyl carbon of an aminoacyl phosphate oligonucleotide. Here, employing molecular dynamics simulations, we examined the possible mechanisms that determine this chiral selectivity. The simulation system adopted a geometry required for the chemical reaction to occur more frequently with L-alanine than that with D-alanine. For L-alanine, the structure with this geometry was formed by a combination of stable dihedral angles along alanyl phosphate backbone with a canonical RNA structure, where the methyl group of alanine was placed on the opposite side of the approaching 3′-hydroxyl group with respect to the carbonyl plane. For D-alanine, the methyl group and the 3′-hydroxyl group were placed on the same side with respect to the carbonyl plane, which significantly decreased its ability to approach 3′-oxygen close to the carbonyl carbon compared to L-alanine. The mechanism suggested herein can explain experimentally observed chiral preferences.

Issue Section: Chemical Biology and Nucleic Acid Chemistry

Darwin, durma com um barulho desses: as celebridades foram convocadas para alavancar maior aceitação da teoria da evolução na sociedade!

quarta-feira, novembro 28, 2018

Celebrity Opinion Influences Public Acceptance of Human Evolution

Steven Arnocky, Emma Bozek, Caroline Dufort, Samantha Rybka, Robyn Hebert

First Published September 19, 2018 Research Article 


Article information 

Article has an altmetric score of 118 Open Access Creative Commons Attribution, Non Commercial 4.0 License

Article Information

Volume: 16 issue: 3,

Article first published online: September 19, 2018; Issue published: July 1, 2018 

Received: July 06, 2017; Accepted: August 21, 2018

Steven Arnocky1, Emma Bozek1, Caroline Dufort1, Samantha Rybka1, Robyn Hebert1

1 Nipissing University, North Bay, Ontario, Canada

Corresponding Author: Steven Arnocky, Department of Psychology, Nipissing University, 100 College Drive, North Bay, Ontario, Canada P1B 8L7. Email: stevena@nipissingu.ca

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

Source/Fonte: Justin Bieber, by Lou Stejskal [CC BY 2.0], via Wikimedia Commons.

Abstract

The present research examined the influence of celebrity opinion upon individuals’ acceptance of the theory of evolution. Priming stimuli were developed purveying pro-evolution, anti-evolution, or neutral opinion (Study 1). When paired with a male celebrity or expert source (Study 2), the male celebrity, but not the male expert, influenced undergraduates’ acceptance of evolution. The influence of the male celebrity on acceptance of evolution was replicated in a community sample (Study 3). When paired with a female celebrity source, undergraduates’ acceptance of evolution was similarly influenced (Study 4). Together, these findings extend our understanding of the reach of credible celebrity endorsers beyond consumer behavior to core individual beliefs, such as those surrounding the acceptance of human evolution.

Keywords celebrity, interpersonal influences, social influences, theory of evolution, religiosity, attitudes

FREE PDF GRATIS: Evolutionary Psychology

O oxigênio poderia estar disponível para a vida tão cedo quanto 3.5 bilhões de anos atrás

Early Archean origin of Photosystem II


Tanai Cardona, Patricia Sánchez‐Baracaldo, A. William Rutherford, Anthony W. Larkum

First published: 09 November 2018
https://doi.org/10.1111/gbi.12322

image

Abstract

Photosystem II is a photochemical reaction center that catalyzes the light‐driven oxidation of water to molecular oxygen. Water oxidation is the distinctive photochemical reaction that permitted the evolution of oxygenic photosynthesis and the eventual rise of eukaryotes. At what point during the history of life an ancestral photosystem evolved the capacity to oxidize water still remains unknown. Here, we study the evolution of the core reaction center proteins of Photosystem II using sequence and structural comparisons in combination with Bayesian relaxed molecular clocks. Our results indicate that a homodimeric photosystem with sufficient oxidizing power to split water had already appeared in the early Archean about a billion years before the most recent common ancestor of all described Cyanobacteria capable of oxygenic photosynthesis, and well before the diversification of some of the known groups of anoxygenic photosynthetic bacteria. Based on a structural and functional rationale, we hypothesize that this early Archean photosystem was capable of water oxidation to oxygen and had already evolved protection mechanisms against the formation of reactive oxygen species. This would place primordial forms of oxygenic photosynthesis at a very early stage in the evolutionary history of life.

Keywords
Archean Chloroflexi Cyanobacteria evolution photosystem Proteobacteria 
reaction center water oxidation

Funding Information
Imperial College London
Leverhulme Trust. Grant Number: RPG‐2017‐223
Royal Society
Biotechnology and Biological Sciences Research Council. Grant Numbers: BB/K002627/1, BB/L011206/1

Publication History
Version of Record online: 09 November 2018
Manuscript accepted: 11 October 2018 Manuscript revised: 03 October 2018
Manuscript received: 13 September 2018

FREE PDF GRATIS: Geobiology

Novo código genético descoberto!!!

terça-feira, novembro 27, 2018

Mitogenomics reveals a novel genetic code in Hemichordata


Yuanning Li Kevin M Kocot Michael G Tassia Johanna T Cannon Matthias Bernt Kenneth M Halanych

Genome Biology and Evolution, evy254, https://doi.org/10.1093/gbe/evy254

Published: 23 November 2018

Article history

Received: 02 July 2018 Revision Received: 20 September 2018

Accepted: 13 November 2018 


Source/Fonte: Graptolite.net


Abstract

The diverse array of codon reassignments has demonstrated that the genetic code is not universal in nature. Exploring mechanisms underlying codon reassignment is critical for understanding the evolution of the genetic code during translation. Hemichordata, comprising worm-like Enteropneusta and colonial filter-feeding Pterobranchia, is the sister taxon of echinoderms and is more distantly related to chordates. However, only a few hemichordate mitochondrial genomes have been sequenced hindering our understanding of mitochondrial genome evolution within Deuterostomia. In this study, we sequenced four mitochondrial genomes and two transcriptomes, including representatives of both major hemichordate lineages and analysed together with public available data. Contrary to the current understanding of the mitochondrial genetic code in hemichordates, our comparative analyses suggest that UAA encodes Tyr instead of a “Stop” codon in the pterobranch lineage Cephalodiscidae. We also predict that AAA encodes Lys in pterobranch and enteropneust mitochondrial genomes, contradicting the previous assumption that hemichordates share the same genetic code with echinoderms for which AAA encodes Asn. Thus, we propose a new mitochondrial genetic code for Cephalodiscus and a revised code for enteropneusts. Moreover, our phylogenetic analyses are largely consistent with previous phylogenomic studies. The only exception isthe phylogenetic position of the enteropneust Stereobalanus, whose placement has been unstable in previous studies, as sister to all other described enteropneusts. With broader taxonomic sampling, we provide evidence that evolution of mitochondrial gene order and genetic codes in Hemichordata are more dynamic than previously thought and these finding provide insights into mitochondrial genome evolution within this clade. 


genetic codon reassignment, Hemichordata, Deuterostomia, mitogenomics

Issue Section: Research article


© The Author(s) 2018. Published by Oxford University Press on behalf of the Society for Molecular Biology and Evolution.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com 


FREE PDF GRATIS: Genome Biology and Evolution
 
Supplementary Data - docx file