If one thing is for sure, it is mitochondrion’s ascending career in late biology. Mitochondria are the power centers of the eukariotic cell and eventually tell the nucleus what to do next: die or live. Mitos do not exist stably as distinct, individual, autonomous organelles according to new results, but form a highly dynamic semi-tubular network.
Mitochondria are bacterium size, membrane-bound organelles in the eukaryotic cell and were descended from prokaryotic endosymbionts about two billion years ago.
Mitos are the main energy supplier, the power centers of the eukariotic cell, in the form of ATP, the vast majority of cellular Reactive Oxigen Species (ROS, oxidants), approximately 90% can be traced back to the mitochondria. The main apoptotic signals of programmed cell death come from there, so eventually mitochondria tell the cell (i.e. the nucleus) what to do next: die or live.
In the past decade a new concept of mitochondrial presence and spatial distribution in the host cell was articulated based on microscopy observation, which suggested the fusion and fission of different mitochondria: the mitochondrial network concept. Mitochondria form a highly dynamic semi-tubular network in the cell, the morphology of which is regulated by movements along the cytoskeleton and the balance of mitochondrial fusion and fission events. Recent developments identified some essential protein players in fusion and fission machinery of mitochondria in eukaryotic cells, like GTPases, Mfn1, Mfn2 in fusion and Drp1 in fragmentation. According to the new network mitochondrion concept, mitochondria do not exist stably as distinct, individual, autonomous organelles. Rather, mitochondria form a network within cells; their continous fusion and fission is a highly dynamic process, adapting to the role the mitochondrion actually has in the cell. Increasing results confirm the role of mitochondrial fission and fragmentation in most forms of apoptosis, even as a cause. This suggests that fragmented mitochondria are in a „bad“ condition, under oxidative stress. Conversely, for example fragmentation of mitochondria in hippocampal neurons seems to have a role in the proper function of neuronal protrusions. On the other hand, mitochondrial fusion is thought to have a role in the maintenance of correct mitochondrial function.
So if you ask a cell, what she intends to do, you’d better ask and take a look at her mitochondria first.
In regenerative medicine mitochondria’s role will be much more important as we become more and more familiar with their tricks. In my opinion a whole new and powerful subfield will arise in biomedicine, organellar therapy, which is subcellular (not cell transplantation) and supramolecular (not classical pharmacology).
Picture: (Human stem cell stained with Mitotracker Red, which specifically bind to mitochondria, visualized in a black-and-white retro style. You can see the mitochondrial structure of the cell, mitochondria in an elongated form. Author’s shot.)