Alfredo Leonardo Porfirio de Sousa

Welcome to this [under construction] personal, yet communal, page. Each essay below deals about a fundamental issue proposed and discussed in the course: "Principles of molecular evolution applied to phylogenetic reconstruction". Each essay has two versions. I wrote the original versions after each class based on the literature and class discussions. Classmates contributed with the revised versions by commenting, editing, and criticizing the original ones. Our aim is to present some fundamental issues related to molecular biology, evolution, and/or phylogenetic reconstruction, as objective and clear as possible. Thus, this personal page is a communal production based on scientific literature and class discussions.

Optional Essay - March, 10th

The central dogma of molecular biology and the endosymbiotic theory

The central dogma of molecular biology conceptually bases the endosymbiotic theory. Sequential information transference is the center idea of the dogma. It deals with information from one type of alphabet (DNA, RNA or Protein) being transferred to another type of alphabet. Endosymbiosis theory states that mitochondria and plastids descent from prokaryotic lineage organisms. We can define two main kinds of information transfer related to endosymbiosis establishment. The first kind is the gene transfer from the symbiotic prokaryote to the host cell nucleus, which creates a dependence of the prokaryotic organism for its host. The second kind is the sequential information transfer from the nucleus DNA, through RNA, to proteins that are functional at the mitochondria or plastids. The information transfer and the interdependence between different organisms during endosymbiosis establishment and conservation were possible since they share the same basic information transfer patterns and alphabets. Thus, endosymbiosis turns to be a plausible proposal in the light of the central dogma of Molecular Biology, with countless evidences nowadays.


*CORREÇÃO FEITA POR: Rosana Fernandes da Cunha
Sua "topic sentence" está bem evidente, no primeiro período eu já soube do que se tratava toda a explicação do seu parágrafo, isso ajudou bastante. Essa frase ficou estranha: "It deals with information from one type of alphabet (DNA, RNA or Protein) being transferred to another type of alphabet." Informação de um tipo de alfabeto para outro tipo de alfabeto? O termo alfabeto poderia ser substituído. Achei interessante a ideia de trazer um exemplo da temática além daquilo que foi explicado em sala de aula. Estou partindo do pressuposto que sua informação é verdadeira, mas peço que da próxima vez você referencie para que os colegas que não saibam dos dados (como eu!), possam dar uma lida e fazer uma critica mais embasada do seu argumento. As frases estão bem construídas, sentenças curtas e com poucos verbos, isso facilita a leitura e entendimento do seu raciocínio. Parabéns pelo texto!


The central dogma of molecular biology and the endosymbiotic theory - Revised version

The central dogma of molecular biology conceptually bases the endosymbiotic theory. Sequential information transference is the center idea of the dogma [1]. It deals with information from one type of residue (DNA, RNA or Protein) being transferred to another type of residue [1](Figure 1). Endosymbiosis theory states that mitochondria and plastids descent from prokaryotic lineage organisms [2]. We can define two main kinds of information transfer related to endosymbiosis establishment. The first kind is the gene transfer from the symbiotic prokaryote to the host cell nucleus, which creates a dependence of the prokaryotic organism for its host [3]. The second kind is the sequential information transfer from the nucleus DNA, through RNA, to proteins that are functional at the mitochondria or plastids [3]. The information transfer and the interdependence between different organisms during endosymbiosis establishment and conservation were possible since they share the same basic information transfer patterns and alphabets. Thus, endosymbiosis turns to be a plausible proposal in the light of the central dogma of Molecular Biology, with countless evidences nowadays [3 4 5 6].


Essay 1 - March, 17th

PCR artefacts and molecular studies

Polymerase chain reaction (PCR) artefacts can impair molecular studies. PCR is a method that mimics DNA replication in vitro [7]. This technique enables to obtain high concentrations of an specific DNA sequence from a small amount of extracted DNA [7], for further sequencing. Just like in vivo DNA replication, PCR is not immune from errors. Different kinds of replication errors can occur during PCR [8], like: base substitution, base addition, base deletion and (PCR-mediated) recombination [9]. These PCR errors can fuzzy sequence analysis or even be misinterpreted as real mutations from organisms. However, PCR optimization reduces these artefacts [see 9 as an example] and biological replicates enables to identify PCR errors. Since PCR errors are random, it is unlikely to find exactly the same error in different biological replicates. Thus, PCR artefacts can impair molecular studies while PCR optimization and biological replicates improve it.


Correção Essay 1 by Domingo Lago: A palavra 'fuzzy' que você usa na frase "These PCR errors can fuzzy sequence analysis or even be misinterpreted…" é uma forma muito casual de falar. Pode usar palabras como 'altered' ou 'modify'. Si alguma vez precisa de encontrar sinônimos em inglês, procure na internet um "Thesaurus" que vem a ser um dicionário de sinonimos em inlês.
O resto do ensaio acho que presenta frases cortas, claras e concretas.


PCR artefacts and molecular studies - Revised version

Polymerase Chain Reaction (PCR) artefacts can impair molecular studies. PCR is a method that mimics DNA replication in vitro [7]. This technique enables to obtain high concentrations of an specific DNA sequence from a small amount of extracted DNA [7], for further sequencing. Just like in vivo DNA replication, PCR is not immune from errors. Different kinds of replication errors can occur during PCR [8], like: base substitution, base addition, base deletion and (PCR-mediated) recombination [9]. These PCR errors can impair sequence analysis or even be misinterpreted as real mutations from organisms. However, PCR optimization reduces these artefacts [see 9 as an example] and biological replicates enables to identify PCR errors. Since PCR errors are random, it is unlikely to find exactly the same error in different biological replicates. Thus, PCR artefacts can impair molecular studies while PCR optimization and biological replicates improve it.


Essay 2 - March, 24th

Allele fixation by genetic drift

New-allele fixation by genetic drift is not an improbable event. Genetic drift is the stochastic allele frequency variation through time [10]. This stochastic variation can exclude, maintain, or even fixate a new allele. However, biologists neglected the importance of stochastic events in evolution. Based on adaptationist ideas during the 70’s, they believed that allele fixation mainly occurs by natural selection of adaptive variations. Consequently, researchers considered stochastic events improbable to explain evolutionary patterns. The skepticism was based on a key question: How could a new allele with no function or better function be fixated in a population? The answer is related with two aspects of populations genetic evolution: Rate of new allele appearance and population size. New alleles appear frequently in populations due to the high nucleotide substitutions rate, as discussed by kimura [11]. In this context, with a lot of new alleles appearing in a finite population the fixation of some of these new alleles become more intuitive than previously. Nowadays, diverse literature corroborates that genetic drift is one of the forces related to evolution. We can mathematically model and test if genetic drift explains an pattern observed. Thus, new allele fixation by genetic drift is improbable in an adaptationist point of view but it frequently occurs in natural populations.

Correção feita por Lyslaine Hatsue Sato:
O seu ensaio está escrito de forma clara e objetiva. O topic sentence no inicio do paragrafo apresenta a ideia de que trata o seu texto.

Essay 3 - March, 31

Target audience: Biology undergraduate students attending to Population genetics course.

Effective population size and genetic drift

The genetic drift relevance is determined by the effective population size (Ne). Genetic drift is the stochastic allele frequency variation through time in a population [10]. This stochastic variation is more significant in populations of small size. But it is not the number of individual (census) that determines a big or small sized population in genetic context. Since genetic drift deals with allele frequencies, it is the “genetic size” of the population that would affect genetic drift. The Ne is the population size measure that considers the genetic diversity and not the number of individual. Thus, we look at the Ne to consider if a population is a big or small to genetic drift.

Bibliography
Optional Essay
1. Crick, F. (1970). Central dogma of molecular biology. Nature, 227(5258), 561-563.
3. Timmis, J. N., Ayliffe, M. A., Huang, C. Y., & Martin, W. (2004). Endosymbiotic gene transfer: organelle genomes forge eukaryotic chromosomes. Nature Reviews Genetics, 5(2), 123-135.
4. Zimorski, V., Ku, C., Martin, W. F., & Gould, S. B. (2014). Endosymbiotic theory for organelle origins. Current opinion in microbiology, 22, 38-48.
5. Lin, Z., Kong, H., Nei, M., & Ma, H. (2006). Origins and evolution of the recA/RAD51 gene family: evidence for ancient gene duplication and endosymbiotic gene transfer. Proceedings of the National Academy of Sciences, 103(27), 10328-10333.
6. Hofstatter, P. G., Tice, A. K., Kang, S., Brown, M. W., & Lahr, D. J. (2016, October). Evolution of bacterial recombinase A (recA) in eukaryotes explained by addition of genomic data of key microbial lineages. In Proc. R. Soc. B (Vol. 283, No. 1840, p. 20161453). The Royal Society.
Essay 1
7. Mullis, K., Faloona, F., Scharf, S., Saiki, R. K., Horn, G. T., & Erlich, H. (1986, January). Specific enzymatic amplification of DNA in vitro: the polymerase chain reaction. In Cold Spring Harbor symposia on quantitative biology (Vol. 51, pp. 263-273). Cold Spring Harbor Laboratory Press.
8. McInerney, P., Adams, P., & Hadi, M. Z. (2014). Error rate comparison during polymerase chain reaction by DNA polymerase. Molecular biology international, 2014.
Essay 2
10. Ridley, M. (2009). Evolução. Artmed Editora.
11. Kimura, Motoo (1968) Evolutionary Rate at the Molecular Level. Nature, 217:624.
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