Rosana Fernandes da Cunha

Ensaio opcional - 10/03/17

The central dogma of molecular biology, proposed by Crick in 1958, deals with the transmission of genetic information in biological systems. In this flow of information the same message is encoded from different ways. However, as dogma itself has already emphasized, and several studies of this phenomenon later, once this information has passed into protein, it cannot be further recoded into RNA or DNA again. An amino acid (unit that forms the proteins) can be encoded by more than one codon (triplet of bases). In observing amino acids, it is noted that the nucleotides of the third position of the codon undergo a high mutation rate (mainly because of the conformation of the ribosome in the third base, which facilitates the modification of the last nucleotide of the triplet), and this change may or may not generate a new amino acid in the protein sequence. For example, proline can be encoded by four different codons (CCA, CCC, CCG, CCU), if only the nucleotide of the last position undergoes a mutation, the amino acid will remain proline and there will be no change in the formation of the protein. This process will create a "noise" in genetic analysis. But what these different rates of mutations in the nucleotides of an amino acid can tell us about the dogma? Who performs and undergoes evolutionary pressures are the proteins and what they do. Its genetic sequences are less conserved and susceptible to higher mutation rates, which makes it difficult for a protein to decode the genetic sequence of RNA and/or DNA that gave rise to it, corroborating the premise of dogma that the transfer of information from proteins to RNA or DNA does not exist. From the above, it is concluded that, despite more than 50 years of its formulation, central dogma remains crucial in the interpretation of molecular phenomena and serves as a subsidy for current (and future) works on the transfer of genetic information.

Revisado por: Alfredo de Souza

The central dogma of molecular biology, proposed by Crick in 1958, deals with the transmission of genetic information in biological systems (Não parece ser a ideia central, Topic sentence). In this flow of information (virgula?) the same message is encoded from ("From" -> "in") different ways. However, as (the) dogma itself has already emphasized, and several studies of this phenomenon later, once this information has passed into protein, it cannot be further recoded into RNA or DNA again. An amino acid (unit that forms the proteins) can be encoded by more than one codon (triplet of bases). In (Retirar o "In") observing amino acids, it is noted that the nucleotides of the third position of the codon undergo a high mutation rate (mainly because of the conformation of the ribosome in the third base, which facilitates the modification of the last nucleotide of the triplet), and this change may or may not generate a new amino acid in the protein sequence (Talvez esta seja a ideia da Topic sentence). For example, proline can be encoded by four different codons (CCA, CCC, CCG, CCU), if only the nucleotide of the last position undergoes a mutation, the amino acid will remain proline and there will be no change in the formation of the protein. This process will create a "noise" in genetic analysis. But what these different rates of mutations in the nucleotides of an amino acid can tell us about the dogma? Who performs and undergoes evolutionary pressures are the proteins and what they do. Its genetic sequences are less conserved and susceptible to higher mutation rates, which makes it difficult for a protein to decode the genetic sequence of RNA and/or DNA that gave rise to it, corroborating the premise of dogma that the transfer of information from proteins to RNA or DNA does not exist. From the above, it is concluded that, despite more than 50 years of its formulation, central dogma remains crucial in the interpretation of molecular phenomena and serves as a subsidy for current (and future) works on the transfer of genetic information.

Comentários gerais:
- A ideia central foi bem escolhida. A discussão sobre código degenerado é bastante pertinente e interessante para o tema que estamos trabalhando. A ideia geral passada pelo parágrafo esta bem embasada em conceitos fundamentais da biologia molecular.
- O parágrafo não possui uma Topic sentence. Isso dificultou identificar qual a mensagem central apresentada ou defendida no texto;
- A ideia central aparece no meio do texto e sem muita relação com as frases anteriores. A ideia de discutir o código degenerado apareceu de surpresa, talvez pudesse fazer parte da primeira sentença do parágrafo;
- Algumas frases longas dificultaram a compreensão. Maior números de pontos podem auxiliar nesta questão;
- Os pontos discutidos no desenvolvimento não remetem de forma clara e direta à conclusão. Algumas frases apresentadas no texto não adicionaram informações necessárias para a compreensão da ideia central. Tais informações a mais desviam o foco e diluem o poder dos argumentos centrais.**


Ensaio 1 - 17/03/17

Proofreading is a repair performed by DNA polymerase itself, in this process it detects whether a nucleotide has been added incorrectly, removes it and adds the correct one before continuing DNA synthesis, but not all polymerases have this function. Why does it happen? What would be the advantage of not having a repair tool? It sounds crazy! When we think that many degenerative and lethal mutations cease to be expressed because the repairing machinery, it is even difficult to believe that there are organisms that "prefer" not to have it in their composition. However, they do exist! Some Bacteria and Archaea do not present proofreading in their DNA polymerases. For these organisms, which want to have a gigantic population, maintaining mutation errors can be beneficial. How can this be positive? The number of organisms in these populations is very large, the conservation of high error rates can end up generating a "successes" that, from generation to generation, becomes an evolutionary gain. Due to the large number of individuals in these populations, this process ends up being feasible, since the loss of organisms does not affect their maintenance. The eukaryotic repair machinery, however, is more refined. Because they are smaller populations, they can not afford the "luxury" of losing their organisms, this diminishes the reproductive power and the gene flow among individuals, which can lead them to extinction!

Revisado por: Lyslaine Sato

A ideia to texto foi bem desenvolvida
Os questionamentos ao longo do texto proporcionam uma discussão interessante e uma abordagem informal ao tema, que deve ser adotado com cautela de acordo a finalidade do texto
Poderia ter sido utilizado ponto final ao expor o seu topic sentence.


Ensaio 2 - 24/03/17

The neutral theory proposes that patterns exist without the need of the natural selection, and that 99% of them are caused only by stochastic events. Kimura (1968) proposed that the variations found in organisms are formed from processes of mutation and genetic drift, not by natural selection, as was widespread. In genetic drift the mutations are random over time and lead to a more or less predictable result. That is, you know what will happen, but you do not know the exact trajectory of this event. From these ideas the neutral theory allowed hypotheses to be created for molecular substitutions. The null hypothesis will always be that the substitutions are neutral, that is, non-adaptive. The alternative hypothesis is that they are selective, that is, they have adaptive value. This last one generates some alteration that benefits the organism and this one is passed to the next generations. What is known today is that most mutations are deleterious, slightly deleterious, or neutral, mostly neutral. This means that: most mutations do not make a difference or generate some kind of change in the individual, let's say they are "silent".

- Kimura, M. 1968. Evolutionary Rate at the Molecular Level. Nature, 217:624.

Revisado por: Beatriz Gomes

O texto está muito bom, Rosana.
Frases na ordem direta, linguagem clara e concisa. A escrita em inglês está bem fluida, parabéns!


Ensaio 3 - 31/03/17

PÚBLICO ALVO: Estudantes de Pós-graduação

Effective population size deals with how many individuals are effectively contributing to the genetics of the next generations (Ballou & Foose, 1996). The measure of this parameter is made from the genetic diversity found in the alleles. Within a population, the greater the number of heterozygotes, the more diverse it is. In a small population, heterozygosity is lost quickly, as genetic drift acts faster. In larger populations, the drift effect is more buffered and occurs more slowly. In these, genetic drift loses its "power" to fix new alleles. However, even in large populations, when there are individuals who interbreed, the tendency of this population is to become increasingly homozygous over time. Another important point to emphasize is that allele fixation is random in small populations. However, genetic analysis of subpopulations can "forge" a high heterozygosity that does not exist, which creates a bias in the interpretation of the data. Natural selection does not act on small populations. On the other hand, in large populations you can see that a small selective effect can cause significant changes in allele fixation.

- Ballou, J.D. & Foose, T.J. 1996. Demographic and geneticmanagement of captive populations. - In: Kleiman,D.G., Lumpkin, S., Allen, M., Harris, H. & Thompson,K. (Eds.); Wild mammals in captivity. Chicago, Univer-sity of Chicago Press, USA, pp. 263-283.

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