Mitochondria are mixed during cell division

In 1855, the German physician Rudolf Virchow coined the phrase Omnis cellula e cellula — all cells come from cells. In other words, cells arise from the growth and division of existing cells. The genetic information stored in chromosomes is passed on to the next generation during cell division in a highly ordered process called mitosis. Biologists have spent many decades deciphering the molecular choreography of this fascinating process, but much less attention has been given to the inheritance of organelles called mitochondria. These are essential for energy metabolism and, because they cannot be generated de novo, they must be inherited, too, Moore et al. describe this process in an unprecedented level of detail. Two major constituents of the cytoskeleton (a network of proteins that determines cellular architecture) are responsible for cellular dynamics. These are microtubules, structures that serve as tracks for long-distance transport of organelles; and actin filaments, which mediate transport over short distances and enable shape changes at the cell’s outer boundary in a region called the cortex. The cytoskeleton is drastically remodelled during cell division. Microtubules build a structure called the mitotic spindle that is needed to partition the chromosomes as the cell divides, and, later, actin filaments assemble a contractile ring that promotes cell separation. Organelles are also extensively remodelled during mitosis. Mitochondria often form extended connected networks in human cells, and these mitochondria fragment into numerous small entities that lose their connection to microtubules during cell division. It has long been thought that the partitioning of mitochondria as cells divide is a largely passive process, but this view is currently changing.

Figure 1

Fig: How mitochondrial organelles are distributed during cell division.

The authors describe three modes of interaction between mitochondria and actin during mitosis (Fig. 1). Previous work suggested that the myosin motor protein Myo19 dynamically tethers mitochondria to an actin network and maintains the distribution of mitochondria throughout the cytoplasm. First, Moore and colleagues observed this process in greater detail than had been reported previously, and found that it is independent of the presence of actin waves. Second, within a wave, mitochondria are encased by what looks like clouds of actin filaments that seem to immobilize the organelles. And third, sometimes these clouds ‘opened’, to be followed by an astonishing burst of mitochondrial movement. The organelles were propelled by the rapid growth (polymerization) of actin filaments. This generated what looks like a comet tail made of actin. These mitochondrial movements were rapid, randomly oriented, and covered substantial distances in the cell.

Moore and colleagues’ observation of actin comet tails is particularly exciting. Two decades ago, it was suggested that actin polymerization drives mitochondrial motility in yeast cells However, this model is controversial because the transport of mitochondria into the bud that forms when yeast divides is mediated by a myosin motor protein ‘walking’ along actin cables, and mitochondrial comet tails of actin have not been documented in yeast. Nevertheless, movement that relies on actin dynamics is quite common in animal cells. Such processes contribute to the internalization of vesicles, and actin is hijacked by certain invading microorganisms to enable them to move in the cytoplasm of a host cell.

Certain types of cell divide asymmetrically and generate daughter cells with different fates. During the division of a stem cell, the older mitochondria in the dividing cell are preferentially partitioned to the daughter cell that is destined to differentiate, whereas the younger and ‘fitter’ mitochondria are apportioned to the daughter cell that maintains stem-cell properties. One can predict, therefore, that mitochondria mixing is suppressed in these cells and that other, as yet unknown, mechanisms ensure the asymmetric inheritance of mitochondria. Clearly, mitochondrial research will yield many more surprises in the future.

https://doi.org/10.1038/d41586-021-00511-3

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