Two recent articles that I came across clearly illustrate ways in which cellular asymmetry is both easily established by basic factors, and provide the basis for processes like cellular polarity and aging. One cannot claim with certainty what these findings in mathematical models and yeast, respectively, impart to our understanding of human health. But they do allow us to generally describe very basic rules for the operation of eukaryotic life.
In the first, Steven Altschuler and colleagues at the University of Texas SW demonstrated in a modeling study the spontaneous emergence of cell polarity. They demonstrate that chance recruitment of a given signaling molecule to sites at the cell’s membrane where it is already bound – a positive feedback – is sufficient to provide the basis for polarity, provided that the total pool of this molecule is small. When the number of molecules becomes too high, other biological mechanisms such as cytoskeleton-based transport are needed.
In the second article, Zhanna Shcheprova and coworkers in Zurich, Switzerland, illustrate a mechanism for asymmetric segregation of age during yeast budding. They show that a diffusion barrier develops in the nuclear envelope of the dividing yeast nucleus. The barrier prevents pre-existing nuclear pores and other membrane-associated proteins from moving into the bud.
This second article provides an excellent example of the spontaneous emergence of asymmetry/polarity, and an example of its function (i.e. cell aging). In this case though, cytoskeleton-based transport is replaced with compartmentalization – really a variation on transport.
And that’s really what the aging article shows – a variation on a biological “rule” that’s been uncovered. It could have turned out any number of ways, and now that it seems so patently obvious, it almost seems like a tautology. But it’s not. Polarity didn’t have to be generated by diffusion.
At the level of our basic building blocks, complex life changes such as aging, locamotion, and others, are becoming rather, well, simple.
Image: Figure 1 from Altschuler et al., Nature
Altschuler SJ, Angenent SB, Wang Y, Wu LF, Nature. 454:886-889 (14 Aug 2008)
Shcheprova Z, Baldi S, Frei SB, Gonnet G, Barral Y, Nature. 454:728-734 (7 Aug 2008)
Normal cells are unable to replicate past several rounds of proliferation (termed the Hayflick limit) as with each round of proliferation the telomeres shorten. When the telomeres reach a critically reduced length, DNA damage is triggered leading to cellular senescence. Therefore, if you tried to culture a primary cell population it would eventually die unless […]
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