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Guest Lecture - Maggie Werner-Washburne

Lauren Erica Davis

Last week Maggie talked to us about Mitochondria. We discussed the four approaches use to look at mitochondria, 1. Cell biology 2. Biochemistry, 3. Genetics, 4. Molecular Biology. We then talked about diseases which affect mitochondria which are serious because of the crucial role of mitochondria in powering the cell and their role in apoptosis.

Maggie then led us on an imaginary tour of the cell and the mitochondria and we explored the problem of keeping an H+ gradient when the pores on the cell membrane are open. We decided that the solution is the the inner membrane is static and that membrane proteins can interact creating sealed pockets in which the H+ gradient can be maintained. And then we discussed the problem with the current way of teaching biology using models which gives the impression that cells are static which they are not.

We also discussed the equation for Gibbs free energy under standard conditions which equals -RTlnKeq which works when the conditions are static, but in biological systems the conditions are constantly changing so a better equation for biology is deltaG=-RTlnKeq+RTln([product]/[reactants]) where the products and reactants are constantly changing. Therefore the conversion of ATP to ADP can yield more energy when the concentration of ATP is high and ADP is low and the conversion of ADP to ATP can require less energy when the concentration of ADP is high and ATP low. We also discussed logs and no one knew their logs and we talked about how biologists need to know math because it is important and little is importance is placed on math for biology majors.

Then we talked about yeast and the assumption that the measurements we get are a representation of what is going one in each cell when really the measurement is an average of all the cells together. So again our assumptions color the conclusions we come too and often lead us to the wrong conclusions. So we need to be aware of the assumptions that we are making and consider the alternatives.


  1. Is there a difference in the mitochondria of different cell types or are they all the same?
  2. How is mitochondrial activity controlled? Is there chemical signalling? How are they activated/deactivated?
  3. What causes the inner membrane to move? Is it only controlled by electrostatic interactions or is there an active component as well?

Future directions

  1. I would study the interactions of the proteins in the mitochondrial inner membrane using computational models.
  2. I would look at the flux of chemicals going in and out of mitochondria at different levels of activity to try to determine what was controlling the activity.
  3. I would study the movement of cristae using electron micrographs.