Essay On Mitochondrial Trafficking

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.

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

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

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

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

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,

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 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

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.

Many physiological processes in the cells require the participation of both intra- and extra-mitochondrial enzyme reactions. A link between mitochondria and cytosol is provided by a group of proteins known as the mitochondrial carriers (MCs) family (Arco & Satrustegui, 2005; F. Palmieri, 2004). MCs comprise a family of about 40-50 proteins, depending on the organism, and provide the main communication between mitochondrial matrix and extra-mitochondrial spaces by transporting a wide range of metabolites, nucleotides and cofactors.

This is further supported by the fact that there are comparable numbers of mitochondria distributed at different distances from the soma in WT and RTT neurons. Therefore, WT and RTT mitochondria do reach the synapse, but do so at different velocities. As it takes longer for the RTT mitochondria to reach the synapses, they would have synthesized more ATP before they reached the synapse. This may help explain the cause of synaptic dysfunction in RTT neurons, as the increased demand for ATP to facilitate trafficking will reduce their efficiency in the synapse. Further studies to measure ATP levels at the synapse will need to be conducted to confirm this statement. However, results showed that 5µM SW-100 does not significantly affect mitochondrial velocity in neurons of both genotypes, which indicates that either the drug has no effect on mitochondrial trafficking or higher concentrations are needed.

The ER-mitochondria contact site is a specialized region where the two membranes are tethered closely together without fusing [1]. Visualization

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

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

Mitochondria and chloroplasts have two membranes that surround them. The inner membrane is probably from the engulfed bacterium and this is supported by that the enzymes and proteins are most like their counterparts in prokaryotes. The outer membrane is formed from the plasma membrane or endoplasmic reticulum of the host cell. The electron transport enzymes and the H+ ATPase are only found in the mitochondria and chloroplasts of the eukaryotic cell. (2)