奥克兰assignment代写 ATP6基因

2020-07-27 20:00

ATP6基因提供了制造一种蛋白质的重要信息，而这种蛋白质对典型的线粒体功能至关重要。线粒体的功能是将食物中的能量转化为细胞可以利用的能量。线粒体通过氧化磷酸化过程产生能量，氧化磷酸化是利用氧和糖产生ATP, ATP是细胞的主要能量来源。ATP6只构成更大的整个酶ATP合酶的一部分。ATP合酶是氧化磷酸化的最后一步。在ATP合酶过程中，允许质子通过膜进入线粒体。在线粒体内部，质子被用来将二磷酸腺苷转化为ATP (MT-ATP6基因)。当ATP6基因发生突变时，就会出现健康问题，如母亲遗传Leigh综合征(MILS)和神经病变、共济失调和视网膜色素变性(NARP)。NARP和MILS是由影响线粒体内能量生产的异常引起的遗传疾病。NARP可以被描述为一种受影响的协调运动能力，而MILS可以被描述为一种线粒体紊乱，在全身发现乳酸水平升高。果蝇寿命短，易于操纵基因组，并且与人类中发现的致病基因有很多相同之处，因此在本实验中，果蝇成为了完美的模型生物(Dautant et al.， 2018)。在此实验之前进行的研究表明，黑腹果蝇和人类体内的突变证实了常见的表型，如瘫痪、寿命短得多以及神经肌肉退化。该研究还表明，在患有MILS疾病的人类中也发现了变异的黑腹果蝇的运动障碍、神经功能障碍和肌变性(Celotto et al.， 2006)。根据这个信息,这个实验的假设成立,它将需要更长的时间变异ATP6黑腹果蝇的恢复或起床涡20秒钟的黑腹果蝇与野生型相比没有变异的基因。假设这是由于突变的果蝇具有与人类引起mis和NARP相同的突变基因。疾病发作的症状之一,这意味着苍蝇会爆炸敏感使它们更容易发作导致复苏的时间变得更长时间比野生型飞谁会轻松起来,因为它是不容易发作,因为神经恶化(DiMauro, 2005)。此外，我们还假设，在受到机械应力后，突变的黑腹果蝇会比野生型果蝇跑得慢(运动能力下降)。这是假设，因为有突变基因的果蝇将表现出与人类的mis疾病相同的症状，包括运动障碍和神经功能障碍。运动障碍是指果蝇无法有效地移动，这将导致黑腹果蝇的移动速度比野生型果蝇慢。
奥克兰assignment代写 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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