ASSIGNMENT代寫

奧克蘭assignment代寫 ATP6基因

2020-07-27 20:00

ATP6基因提供了制造一種蛋白質的重要信息,而這種蛋白質對典型的線粒體功能至關重要。線粒體的功能是將食物中的能量轉化為細胞可以利用的能量。線粒體通過氧化磷酸化過程產生能量,氧化磷酸化是利用氧和糖產生ATP, ATP是細胞的主要能量來源。ATP6只構成更大的整個酶ATP合酶的一部分。ATP合酶是氧化磷酸化的最后一步。在ATP合酶過程中,允許質子通過膜進入線粒體。在線粒體內部,質子被用來將二磷酸腺苷轉化為ATP (MT-ATP6基因)。當ATP6基因發生突變時,就會出現健康問題,如母親遺傳Leigh綜合征(MILS)和神經病變、共濟失調和視網膜色素變性(NARP)。NARP和MILS是由影響線粒體內能量生產的異常引起的遺傳疾病。NARP可以被描述為一種受影響的協調運動能力,而MILS可以被描述為一種線粒體紊亂,在全身發現乳酸水平升高。果蠅壽命短,易于操縱基因組,并且與人類中發現的致病基因有很多相同之處,因此在本實驗中,果蠅成為了完美的模型生物(Dautant et al., 2018)。在此實驗之前進行的研究表明,黑腹果蠅和人類體內的突變證實了常見的表型,如癱瘓、壽命短得多以及神經肌肉退化。該研究還表明,在患有MILS疾病的人類中也發現了變異的黑腹果蠅的運動障礙、神經功能障礙和肌變性(Celotto et al., 2006)。根據這個信息,這個實驗的假設成立,它將需要更長的時間變異ATP6黑腹果蠅的恢復或起床渦20秒鐘的黑腹果蠅與野生型相比沒有變異的基因。假設這是由于突變的果蠅具有與人類引起mis和NARP相同的突變基因。疾病發作的癥狀之一,這意味著蒼蠅會爆炸敏感使它們更容易發作導致復蘇的時間變得更長時間比野生型飛誰會輕松起來,因為它是不容易發作,因為神經惡化(DiMauro, 2005)。此外,我們還假設,在受到機械應力后,突變的黑腹果蠅會比野生型果蠅跑得慢(運動能力下降)。這是假設,因為有突變基因的果蠅將表現出與人類的mis疾病相同的癥狀,包括運動障礙和神經功能障礙。運動障礙是指果蠅無法有效地移動,這將導致黑腹果蠅的移動速度比野生型果蠅慢。
奧克蘭assignment代寫 ATP6基因
The ATP6 gene is what provides the vital information to make a protein which is essential for typical mitochondrial function. The function of the mitochondria is to convert energy from food into energy that the cells can utilize to function. Mitochondria produce energy through the process oxidative phosphorylation which is the use of oxygen and sugar to make ATP which is the main source of energy for the cells. ATP6 only forms one part of an even larger whole enzyme, ATP synthase. ATP synthase is the last step during oxidative phosphorylation. Protons are allowed to flow across a membrane during ATP synthase to get inside of the mitochondria. On the inside of the mitochondria is where the proton is used to convert adenosine diphosphate into ATP (MT-ATP6 Gene). When there are mutations within the ATP6 gene, complications can arise with health problems such as maternally inherited Leigh syndrome (MILS) and neuropathy, ataxia and retinitis pigmentosa (NARP). NARP and MILS are genetic disorders caused by abnormalities which are affecting the energy production within the mitochondria. NARP can be characterized as an affected ability to coordinate movements while MILS can be characterized as a mitochondrial disorder with increased levels of lactic acid found throughout the body. The Drosophila Melanogaster made for the perfect model organism in this experiment due to its short lifespan, easy to manipulate genome, and for the fact that is shares most many of the genes found in humans that contribute to disease (Dautant et al., 2018). Studies that have been done prior to this experiment showed that mutations within the Drosophila Melanogaster as well as mutations in humans proved to reveal common phenotypes such as paralysis, a much shorter lifespan, as well as neuromuscular degeneration. The study also showed that the locomotor impairment, neural dysfunction, and myodegeneration found within the mutated Drosophila Melanogaster were also found in humans with the MILS disease (Celotto et al., 2006). Given this information, the hypothesis that was created for this experiment was that it was going to take longer for the mutated ATP6 Drosophila Melanogaster’s to recover or get up from being vortexed for 20 seconds compared to the wildtype of Drosophila Melanogaster that does not have the mutated gene. This was hypothesized due to the mutated flies having the same mutated gene that causes MILS and NARP in humans. One symptom of the diseases is seizures, meaning the flies are going to be bang sensitive making them more susceptible to seizures causing the time for recovery to become much longer than that of the wildtype fly who will get up with ease since it is not susceptible to seizures because of neurological deterioration (DiMauro, 2005). Also, it was hypothesized that the mutated Drosophila Melanogaster will run slower than the wildtype flies (have decreased motility) after receiving mechanical stress. This was hypothesized because the Drosophila Melanogaster that have the mutated gene will show the same symptoms of a human with MILS disease which include locomotor impairment and neural dysfunction. Locomotor impairment is the inability to move efficiently which will cause the Drosophila Melanogaster to move at a slower rate than the wildtype flies.
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