Wednesday, April 6, 2011
Mitochondrias.
Shubin addresses the vital role the mitochondria plays in the functioning of cells, most importantly the conversion of sugar and oxygen into energy (197). Mitochondria's processes have arose from genetic structures with a bacterial past, and gene mutations can be harmful and cause diseases. How do these genetic mutations happen? Recall the different types of distortions that can happen from the gene unit. How do scientists approach to solve diseases such as cardioencephalomyopathy? Also, incorporate mitochondria's history of endosymbiosis.
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Kyle Kim, piece847@gmail.com
ReplyDeleteThe creation of mitochondria is passed down from our mothers. However, mitchondria are created using their own DNA. (This was used as proof of primordial endosymbiosis) However, when even small mutations occur in this DNA it can learn to large, and mostly negative, effects. "If there is a problem in the chemical reactions in which oxygen is consumed, energy production can be impaired. The malfunction may be confined to individual tissues, say the eyes, or may affect every system in the body." (Shubin 197)
ReplyDeleteTherefore, mutations affecting chemical reactions lead to diseases such as cardioencephalomyapathy. There are several ways that this mutation could occur: point mutations (when a single base pair is changed so everything but one codon makes sense), nonsense (where the amino acid is changed into a stop codon), or missense (when a base pair is substituted for another in a part that codes for a protein, changing the amino acid coded for, and thus the protein.) The mutation that would have the most effect would be a base-pair substitution due to the idea of "structure versus function". The mitochondria itself is made of proteins coded by its DNA. If the DNA is changed, it codes for another amino acid, which may alter the overall shape of the protein. If the protein shape is changed, (especially near the active site) it may cause a different substrate to attach to it. In some cases this may create a more effective protein, but in most it just creates a useless protein where a vital one once existed. (Campbell 345) However, scientists are finding ways to find solutions to these diseases by looking at their primordial ancestors. Parococcus denitrificans is the closest free-living relative to mitochondria. By experimenting with its chemical pathway, we are better able to understand diseases such as cardioencephalomyopathy and thus begin to find ways to treat them. (Shubin 198)
Due to the fact that mitochondria are very similar to bacteria in their functioning and development, we can use the known causes of bacterial mutations to think of ways how mitochondria may also mutatate. Bacteria mutate usually in three ways: "some particularly robust cells in a population might adjust to a harsh environment (i.e., adaption);
ReplyDeleteexposure to toxic conditions might produce rare, resistant mutations in a population of bacteria (i.e., induced mutations); or
spontaneous mutants might have ocurred in the bacterial population prior to exposure to toxic conditions, yielding resistant progeny cells (i.e., spontaneous mutations)" (Carpenter, 2004). Given these methods, it seems that mitochondria would be a very sturdy part of the cell that is often resistant to problems such as toxicity, and mutations may often serve them well, as is the case of bacteria. It seems diseases such as cardioencephalomyopathy would happen rarely because of the mitochondria's ability to divide and mutate very frequently, yet problems still persist as they do in bacteria.
Scientists can solve cardioencephalomyopathy as they would with other genetic diseases. When a cell, in this case mitochondria, lacks a certain gene vital for survival, that gene can be introduced into a mitrochondria and injected into cells of the affected tissue. This could be more affective is diagnosis is made during the embryonic stage in which introduced mitochondria make up a bigger proportion of all mitochondria.
http://www.sci.sdsu.edu/~smaloy/MicrobialGenetics/topics/mutations/fluctuation.html
Troy Glickstern
cleverstar8@comcast.net