Extra-Mitochondrial Family Structure

These sequences are sourced from Subunit 1 of the Cytochrome Oxidase gene in the Mitochondria.

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)

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.

Under normal conditions, the mitochondria maintain cytosolic Ca2+ levels, which is necessary for normal cellular function. However, the mitochondrial uptake of excessive levels of Ca2+ can lead to inhibition of ATP synthesis, disruption of mitochondrial membrane potential, increased ROS production, and generation of the mitochondrial permeability transition (mPT) state, which is thought to occur in response to formation of the mPT pore. As a consequence, cellular demise can occur through necrotic-related mechanisms events, including a loss of energy production and oxidative stress as well as apoptotic-related mechanisms, including the mitochondrial release of pro-apoptotic proteins. Given the central role of the mitochondria in cell

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,

Organelles are membrane-bound compartments found within eukaryotic cells that possess specific functions. While they function independently, studies using high-resolution microscopy have shown that organelles such as the endoplasmic reticulum form specialized contact sites with a wide range of cellular structures [1]. One of the most heavily studied organelle contact sites is that between the ER and the mitochondria, which may be involved in lipid biosynthesis, calcium signalling, and mitochondrial division [1]. This paper will first discuss what is known about the structure of these contact sites, and the roles they may play mitochondrial division. A discussion will follow concerning directions for future research to explore the role of phosphatidylinositol in mitochondrial membrane sculpting and fission.

Mitochondria has many key molecules that are present within the organelle. Some of these molecules include oxaloacetate and succinate dehydrogenase, both in which play important roles in cellular respiration. Both of these substrates are essential for the Krebs Cycle, as they both produce ATP within the cycle (Wojtczak, Lech & Wojtczak, A.B. & Ernster, L. 1969). The shape and structure of the molecule oxaloacetate is similar to the components of the molecule succinate dehydrogenase. An active site is part of an enzyme in which a protein or substrate binds to an enzyme (“Active Site.”). Normally,

They provide the energy needed for the cell to carry out their functions. They have a double-layered membrane and have their very own DNA. Importantly, they are involved in immune response. These characteristics make them targets for pathogens.4 Contrary to what one might expect, the bacterial pathogens that target the mitochondria regulate the apoptotic properties of the organelle more so than their immune properties.4 They are able to alter the amount of survival and apoptosis of a cell and use that to their advantage.4 What makes this entire process possible is the bacterial MLS gene.5 These proteins interact with receptors on the mitochondrial membrane and once bound, they initate a signal cascade inside the organelle.5 MLS containing proteins can be found and are active in L.pneumophila. This bacterium does appear to use this strategy in certain situations, but more complete analysis is still required because the process is still

In a single cell there are large numbers of organelles known as mitochondria. These organelles are spherical with a double-membrane, the outer mitochondrial membrane and the inner mitochondrial membrane (Chial). The majority of energy and power for the body’s cells, more than 90% of what is required to preserve life and encourage growth, originates from these organelles in the form of the molecule adenosine triphosphate (Kurt 11; “What”). This energy production process is termed oxidative phosphorylation because it occurs in the presence of oxygen (Sirrs). If there is a fault in this assembling of energy within the mitochondria, it is known as a mitochondrial disease. Usually the organs affected by these diseases are those that require

FOR THE REGULATION of mitochondria biogenesis the nuclear and mitochondrial communication is needed to ensure a correct assemble and activity of the complexes form the electron transport chain (NAderson : Sequence and organization of the human mitochondrial genome)

Mitochondria are double membrane bound organelles that are essential for producing 95% of our cells energy in the form of ATP1. We have around a hundred to a thousand of these organelles present in each of our cells and they are unique to other organelles in that they contain their own DNA1. But why is this? And how has this benefited the cell in evolutionary terms? Mitochondria are most commonly thought of as the ‘power house’ of the cell due to ATP production being their main function however they have also evolved with many other abilities. I plan to focus how the mitochondria came about and how its structure and function have changed. As mitochondria have many functions I will be looking specifically into mitochondria’s roles in ATP production

Under oxygen-restricted conditions, the mitochondrion has undergone reductive alterations of its content and function. These changes were most likely driven by the independence of ATP generation on oxidative phosphorylation in the mitochondria. These reduced mitochondria are called mitochondrion-related organelles (MROs) (9). There are two types which lack mitochondrial DNA--the hydrogenosome and the mitosome. They are distinguished by the fact that the hydrogenosome has retained ATP-generating capacity and the mitosome has not (5). The anaerobic metabolism performed by the hydrogenosome initially suggested that the organelle might have originated through endosymbiosis with an anaerobic bacterium such as Clostridium. It has subsequently been shown that genes for Cpn10, Cpn60, and Hsp70 are present in the nuclear

Mitochondria are double membraned cell organelle that plays central role in cellular energy provision . These organelles have their own genome which is small in size and are transmitted exclusively through female germ line. The human mitochondrial DNA (mtDNA) is a double-stranded, circular and has 16 569 bp which contains 37 genes coding for two rRNAs, 22 tRNAs and 13 polypeptides which are required in oxidative phosphorylation.

Mitochondria are important organelle which is responsible for regulating cellular energy homeostasis and cell death. Hence, the damaged mitochondria could be removed by a mechanism called Mitophagy, which is has particular autophagic elimination mitochondrial (Youle and Narendra, 2011).as the mitochondria are targeted for autophagic degradation (Springer and Macleod, 2016). Furthermore, Mitophagy plays a significant role in cellular homeostasis by eliminating dysfunctional mitochondria and decreasing mitochondrial mass as a response stress. Recent work has linked defect in mitophagy to human diseases such as metabolic disorders diseases (Youle and Narendra, 2011). Furthermore, Metabolic myopathies are inherited or obtained defects in