Researchers at Duke-NUS Medical School have uncovered novel molecular information about how cells control their energy supply to match their energy needs.
The importance of microproteins in the assembly of larger protein complexes inside mitochondria, the energy-producing cell components, is highlighted in their study, which was conducted in collaboration with scientists from Duke University in Durham, North Carolina, and the University of Melbourne in Australia.
The respiratory chain membrane protein complexes and the mitochondrial ATP synthase in the inner membrane cristae work together to convert biological energy in mitochondria.
Recent developments in electron cry microscopy have opened up new perspectives on how these complexes are arranged structurally and functionally in the membrane and how they alter with ageing.
This review examines the essential issues that remain unanswered but can now be explored as well as how these developments fit into the existing body of knowledge.
What Are Mitochondria?
The mitochondria in your cells and consequently, in your body can be compared to the batteries that power them. One of the “organelles” that your cells need to function is the mitochondria, which are found inside your cells.
Your cells require organelles, which are cellular components that support life, much as your body requires certain organs for proper operation (heart, liver, kidneys, etc.).
As almost 90% of the chemical energy your body generates comes from the mitochondria, these tiny organelles are referred to as the “powerhouse” of your cells.
Where do mitochondria receive the substrates that help them produce energy? The mitochondria in your cells are responsible for converting the macronutrients fat, carbohydrates, and protein into energy that can power additional metabolic processes after you eat them.
Simply put, mitochondria are the cell’s energy producers, and when they aren’t functioning well, your body can’t perform their vital tasks as effectively.
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What Do Mitochondria Do?
Despite the fact that producing energy is their most well-known function, mitochondria also perform a number of other crucial functions.
In reality, the genes that make up a mitochondrion’s energy-producing machinery make up only roughly 3 percent of the total genes required to form a mitochondrion. Most of them work in other positions that are unique to the cell type in which they are found.
The complex organic molecule ATP, which is present in all living things, is frequently referred to as the “molecular unit of currency” since it drives metabolic functions. The Krebs cycle or the citric acid cycle are two series of processes that take place in mitochondria to produce the majority of ATP.
On the cristae or folds of the inner membrane, energy is mostly produced. The chemical energy in our meals is converted by mitochondria into a form the cell can utilise. Oxidative phosphorylation is the name of this procedure.
NADH is a substance that is created during the Krebs cycle. Enzymes included into the cristae create ATP using NADH. Energy is conserved as chemical bonds in ATP molecules. The energy can be used to break these chemical bonds.
Apoptosis, another name for cell death, is a necessary process for all living things. Cells are removed and killed when they deteriorate or become damaged.
Which cells are destroyed depends on mitochondria. Cytochrome C, one of the main enzymes responsible for cell death during apoptosis, is released by mitochondria.
It is believed that mitochondria play a role in the disease because certain conditions, including cancer, include a breakdown in normal apoptosis.
Numerous biological activities depend on calcium. For instance, allowing calcium to enter a cell again can cause the release of hormones or neurotransmitters from endocrine or neuronal cells.
Along with other things, calcium is essential for blood coagulation, muscular function, and fertilisation. The cell strictly controls calcium since it is so important. Mitochondria contribute to this process by rapidly collecting calcium ions and storing them until they are required.
Other functions of calcium in the cell include controlling hormone signalling, steroid production, and cellular metabolism.
We shudder to remain warm when it is cold. However, there are other methods for the body to produce heat, and one of them involves the use of a tissue known as brown fat.
Mitochondria have the ability to produce heat through a mechanism known as proton leak. Non-shivering thermogenesis is what is referred to as this. Babyhood, when we are more prone to colds, is when brown fat levels are at their peak; as we age, levels gradually decline.
How A Small Protein Plays A Large Role In Mitochondrial Function?
Mutations in the protein MTCH2 have been linked to Alzheimer’s, Parkinson’s, and leukaemia, but it was unknown how it affected cell function. MTCH2 is essential for building a cell’s mitochondria, specifically for inserting proteins into the mitochondrial outer membrane.
Rebecca Voorhees, assistant professor of biology and biological engineering and Heritage Medical Research Institute investigator, collaborated closely with Jonathan Weissman’s lab at MIT’s Whitehead Institute. Science publishes the study on October 21.
Mitochondria are energy-producing and signaling organelles in cells. The mitochondrial outer membrane helps the cell recognize infections, initiates apoptosis, and breaks down dopamine.
Each protein in the outer membrane is oriented precisely. Without these proteins, mitochondria can’t operate properly, causing a wide range of illnesses. More than 90% of mitochondrial outer membrane proteins are alpha-helical. Researchers have long wondered how they sneak inside the membrane.
New research from the Voorhees and Weissman labs shows that MTCH2 inserts alpha-helical proteins in the right direction into the mitochondrial outer membrane. A large scan of human genes revealed MTCH2’s significance. Experiments showed that MTCH2 is both essential and sufficient for implantation.
“MTCH2 is a mitochondrial outer membrane protein insertase” Caltech’s Alina Guna, Taylor Stevens, and Alison Inglis co-authored the paper.
Joseph Replogle of the Whitehead Institute and UC San Francisco, Theodore Esantsi, Gayathri Muthukumar, Angela Pogson, Caltech graduate students Kelly Shaffer and Maxine Wang, Caltech senior scientist Jeff Jones, former Caltech staff scientist Brett Lomenick, and Tsui-Fen Chou are also coauthors.
Howard Hughes Medical Institute, Human Frontier Science Program, Heritage Medical Research Institute, Larry L. Hillblom Foundation, and NIH provided funding.
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