Essay On Mitochondrial Trafficking

The heavy membrane fraction had the highest percentage distribution (93.236 %) of succinate dehydrogenase, indicating good separation of the mitochondria into their predicted fraction and the success of differential centrifugation as a method of separation. A small percentage of succinate dehydrogenase was also found in the light membrane and cytosolic fractions: 6.131 % and 0.633 % respectively. The activity in these two fractions could be due to excessive homogenisation causing fragmentation of mitochondria into small low-density fragments. The lower density meant they achieved sedimentation at higher centrifugal forces than expected resulting in separation into the light membrane or cytosol fraction (Claude, 1946). Additionally, mitochondrial activity could be present in the light membrane fraction due to disruption of the heavy membrane pellet during transfer of the supernatant, causing the pellet to contaminate the

Mitochondrion function is to produce energy from sugar. This is parallel to a restaurant inside a hospital. The employees eat (carbohydrates) from the hospital restaurant and then their bodies convert it to energy.

The genes which encode for the mitochondria’s component proteins are in 2 separate genetic systems in 2 different locations. One of which is the cell nucleus, but the other is inside the organelle itself. There are relatively few genes inside the

Mitochondria, dubbed the ‘powerhouse of the cell’, are a type of organelle present in most human cells. Their primary function is to generate Adenosine Triphosphate (ATP), the cell’s principal source of chemical energy. Unlike most other organelles, mitochondria store their own set of genetic material, distinct from the DNA situated in a cell’s nucleus. Although this ‘mitochondrial genome’ represents only 0.1% of a cell’s genetic information, it often plays a significant role in development.

A. SIGNIFICANCE. Our goal is to screen chemical libraries to identify compounds that modulate mitochondrial transport in hippocampal and cortical neurons. This study is significant in four ways: (1) There is an urgent need to develop CNS (Central Nervous System) active drugs. CNS disorders are not only staggeringly complex but are poorly treated diseases (Palmer and Stephenson, 2005). In the United States alone the annual cost for stroke, depression, Schizophrenia and Alzheimer’s disease are currently estimated to be over $250 billion annually (Pangalos et al., 2007). Despite the advances in translational medicine and pharmaceutical research little progress has been made in developing CNS therapeutics. Improving CNS drug discovery efforts is an urgent goal as an estimated 1.5 billion people suffer from CNS-related diseases worldwide. Unfortunately only a handful of new drugs have been brought to the market with very few in the pharmaceutical pipeline (Kissinger, 2011; Schoepp, 2011; Abbot, 2011). The majority of pharmaceutical companies have recently announced a shift from supporting internal drug discovery efforts in favor of academic and government partnerships (Schoepp, 2011). At Scripps Florida we have close interaction of state of the art high throughput small molecule screening and cutting-edge neuroscience research. Thus we are in a unique position to address the challenges in developing CNS therapeutics. (2) Mitochondrial dysfunction is part of the pathophysiology of

Electrons are passed between the complexes of the electron transport chain and enable the cells to generate energy. The first complex accepts the electrons that are produced from the degradation of the food we eat. As it passes the electrons to the third complex in the chain protons (positively charged hydrogen atoms) are moved across the inner mitochondrial membrane. At complex three the electrons from complex one are joined by others donated by complex two. Complex three passes these electrons onto complex four and in the process moves more protons across the inner mitochondrial membrane. Within complex four the electrons are joined to oxygen to produce water, alongside one final movement of protons. Since so many protons have now been moved across the membrane the amount of them is higher on one side of the membrane than the other, this creates a gradient. Complex five then uses this gradient to produce ATP. The proton gradient rotates this final complex and with each rotation an ATP is made. For every cycle of the electron transport chain over 30 ATPs are produced, this shows how efficient energy generation is within the

Once a upon time, there was a lonely mitochondria named Sophia Mitochondria. Sophia Mitochondria had been alone for a while and she does not know where her parents are. She want to find her parents so she decided to talk someone to help her which is her childhood best friend, David Chloroplast. However, before she called him, she did her normal routine. She took nutrients from one of their cells, breaks it down and turn it into energy. This routine is also known as cellular respiration. After that, she call her David Chloroplast and thirty minutes later, David Chloroplast was in front of her house. David Chloroplast and Sophia Mitochondria came to Bacteria Garden which Sophia Mitochondria’s parents favorite place to go every weekend. When they

There are hundreds of neurodegenerative diseases (NDD) and the etiology for most of the random conditions remain a universal mystery (Nieoullon 2011). A deterioration of specific functions of the neuron cells of the central nervous system is the most common characteristic of NDD. Neurons are responsible for transmitting essential information to other nerve, muscle and glandular cells (Przedborksi, Jackson-Lewis 2003). Emerging research has recently identified mitochondrial dysfunction as a recurrent elemental link in numerous neurodegenerative disorders (Ghano,

PINK1, encoded by the PINK1 gene, is a part of “quality control” of the mitochondria It finds mitochondria that has been damaged and marks them for autophagy; the controlled digestion of an organelle, in this case, the damaged mitochondria. PINK1 can be taken in and out by healthy mitochondria because of a membrane potential, but damaged mitochondria lack an adequate membrane potential to take in PINK1 protein. The protein will then collect on the outer membrane of the damaged mitochondria, at which point PINK1 will then enlist parkin, another protein associated with Parkinson’s disease, to target the mitochondria for autophagy. The function of PINK1 is not completely known, but because of it’s presence throughout the cytoplasm of cells, a suggestion of the function of PINK1 is to be a lookout for damaged

In the last years, mitochondrial dysfunction and subsequent energy penalty have been hypothesized to drive axonal

The electrons, resulting from the glucose, are transported by the electron carriers, NADH and FADH2, into the electron transport system, which is located in the inner mitochondrial membrane. During stage four, oxidative phosphorylation, electron transport chains change the chemical energy into a form that is required for ATP synthesis in a process referred to as chemiosmosis (the movement of ions through selectively-permeable membrane from an area of higher concentration to an area of lower concentration by transport proteins). Approximately 34 ATPs are formed in this stage. Moving pyruvate and ADP into the mitochondrial matrix and other processes causes some loss of energy. Approximately 32 molecules of ATP are produced from each molecule of glucose degraded to carbon dioxide and water respiration. Each of these molecules contains 7,3/mol of free

The molecule is an important part of the inner part of the mitochondria in which the actual production of the energy occurs.

The hub of energy metabolism, the mitochondrion, is found in virtually all eukaryotic cells, with the exception being erythrocytes. The mitochondrion generates cellular energy in the form of adenosine triphosphate (ATP), mostly by means of the oxidative phosphorylation (OXPHOS) system that is located in the inner mitochondrial membrane. The respiratory chain (CI-CIV) and ATP synthase (CV) is collectively known as the OXPHOS system, encoded by both nuclear DNA (nDNA) and mitochondrial DNA (mtDNA). The number of mitochondria per cell, ranging from hundreds to thousands, is controlled by the energy requirements of specific tissues with the greatest abundance of mitochondria found in metabolic active tissue (Pieczenik and Neustadt, 2007). Mitochondrial disease is caused when there is a defect in any of the numerous mitochondrial pathways, due to spontaneous or inherited mutations. Respiratory chain deficiencies (RCDs) are the largest subgroup of mitochondrial disease and occur when one of the four respiratory chain complexes become impaired. RCDs are considered to be one of the most common

The most prominent cytoplasmic alterations were to the mitochondria. Paracrystalline inclusions were found in many of the mitochondria. These inclusions, are very rare or are non existent in the interfibrillar mitochondria. Each crystalloid is enclosed by a single membrane and at low magnification appeared to be parallel linear densities measuring .34nmin thickness. Higher magnification revealed that the laminae of the crystalloids consisted of linearly arranged dots that were ~34nm in diameter. Some mitochondria, both SSM and IFM, lacked crystalloid inclusions and had few cristae, these particular mitochondria were confined to the organelle periphery where they paralleled the limiting membranes, this left a large area absent of any membranes in the inner compartment. These zones had a variety of different appearances, some mitochondria where completely electron-lucent, others possessed farinaceous material that varied in density, which depended on concentration and packing of electron-dense particles.

Certain mitochondrial DNA mutations have been found to result in mitochondrial dysfunction and have been found to be heavily implicated in the aging process as well as various age-related disorders and diseases. The mutations in the mitochondria can occur in the mother and then be given to the offspring. To conduct the study, the authors used mice to test their theories. The scientists conducting the story wanted to find out just how much the mitochondrial mutations in the DNA could contribute to the rate of aging. They also found something that they didn’t expect, a certain combination of inherited mutations in the mitochondrial DNA can cause stochastic brain malformations. The results that they got from conducting the study indicated that healthy mitochondria may be needed to maintain a certain level of health during