A Lab Notebook

 
Lab Meeting, Kay Bidle
At today's lab meeting Kay Bidle presented his data from the past few months. The first thing he showed, despite Paul's claims otherwise, was a graph of cell number over time in a batch culture. Although the culture was grown in nutrient replete f/2 media, there was a decline in the number of cells after about 10 days. This decline was subsequently followed by another even more populous bloom, of the same species of E. huxleyii. Kay then hypothesized as to why the first bloom died, with such a small number of cells - only to be followed by a larger bloom of the same species. Of particular interest were electron micrographs Kay had from samples prior to and following the peak of the second bloom. If my memory is correct, the organelles of the post bloom cells appeared to be encephalized compared to the pre-bloom cells. Kay then tied this into cell death. Cell death, which can have two forms, either necrosis or apoptosis, is either externall forced or intrinsically wired (repsectively). I have issues with altruism and by inference - group selection ad kin selection. Apoptosis, or Programmed Cell Death (PCD) occurs in all types of cells ranging from unicellular organisms such as phytoplankon, all the way to our own body's cells. In our bodies, PCD occurs numerous times everyday. In fatc, the lack of PCD is commonly manifest as cancer (when cells continue to multiply and will not respond to cues for PCD). However, in phytoplankton commmunities, PCD is viewed by some as an evolutionary advantage. Of course, this is not an advanatge for the individual who succumbs to PCD but is rather an advantage for the remaining members of the population. A selfish gene however has no desire to succumb to PCD such that other genes (individuals in this case) may persist. However, Kay's data showed evidence of caspase activity following infection of a culture by a virus. Increased caspase activity provides a signal for the cell to begin PCD. As a result, the cell will generally lyse (explode, thus killing itself) which will minimize the propagation of the viral infection. The minimization of viral infection relies on the viral strategy of utilizing the transcription machinery of the cell to replicate the viral genetic code. If the cell continues transcription following a viral infection, the virus will soon overtake its host and lyse the cell thus propogating a great number of viral replicates. Obviously, if a cell can die via PCD shortly after infection, it can minimize the extent of viral propagation. That the cell would succumb to PCD following a viral infection relies on the assumption of some sort of altruistic behavior on the cell's behalf. Of course, evolutionary biologists scoff at the idea of an altruistic gene. And, I must agree. It is not in the interest of a unicellular organism to commit suicide and eliminate , on its own, its ability to produce progeny.
While absorbing the end of Kay's talk I devised a silly explanation for such seemingly altruistic behavior. Rather than acting altruistically on behalf of the other members of a species' population, I think the cells the succumb to PCD may in fact be on the losing side of a constant competition for limited resources among all members of a population. I shall explain.
My research is concerned with the constant exudation, by phytoplankton, of extracellular material. In a basic sense this material is hypothesized to be excess photosynthate that leaks as an overflow valve-like mechanism. Now, taking a step back, prokaryotes are known to use quorum sensing to communicate. Such behavior has not yet, to my knowledge, been observed in phytoplankton. As prokaryotes are generally older species than eukaryotes, I do not think it is unreasonable to assume that eukaryotic phytoplankton may utilize similarly complex chemosensing. It is with this in mind that I feel that the exudates of phytoplankton may contribute to PCD. Perchance the exudate from an individual contained discrete chemical cues that that could only be deciphered by another indiviual (of the same species) following a viral infection. My thoughts then proceed: that the viral infection (according to Kay's data) activates caspases (although for wwhat function, we do not know) that react to to specific cues in the exudate of fellow individuals. More plainly put, cells are always exuding potentially lethal cues for their fellow nutrient competitors (other members of the same species) to detect. However, detection of such chemical cues is not possible until an individual's integrity has been compromised, in this case by a virus. This idea, rather than relying on altruistic gene behavior, functions when each gene (individual) is constatntly looking out for themselves by continually emitting a cue to kill compromised competitors, thus increasing the available nutrient pool for itself once the others have died.
Just and incomplete thought on an area of research I know nothing about.
- posted by alex @ 23:17