Mitochondria

The folks who made The Life of the Cell made a new video last year:

Charity Begins with the Cell

As I have argued before, one key to the success of bacteria-as-terraformers is their ability, as single-celled organisms, to network with each other both physiologically and genetically.  Well, recent evidence strongly suggests that such connections also include charitable behavior, where certain cells come to the aid of their neighbors:

Humans are capable of great charity, taking hits to their bank accounts and bodies to benefit their peers. But such acts of altruism aren’t limited to us; they can be found in the simple colonies of bacteria too.

Bacteria are famed for their ability to adapt to our toughest antibiotics. But resistance doesn’t spring up evenly across an entire colony. A new study suggests that a small cadre of hero bacteria are responsible for saving their peers. By shouldering the burden of resistance at a personal cost, these charitable cells ensure that the entire colony survives.

Read the rest about this eye-popping study here.

 

More Explanation for the Missing Prokaryotic Mouse

A few months back, I used the hypothesis of front-loading evolution to outline a subtle, but very important, shift in our perspective of evolution.  Instead of viewing evolution as all about selection picking from a pool of variants, consider the possibility that some variants are more special than others.  In this case, let’s pick a variation that is very special – the complete redesign of the cell plan, as it is this change that was necessary for setting the stage for the emergence of metazoan life.  I explained this as follows:

This is about whether the cell design – the composition and architecture of the prokaryotic cell – is capable of generating something as structurally complex as a mouse (for a mouse, like all animals, is an assembly of cells).  Seen from this angle, the endosymbiotic hypothesis supports my position.  That is, in order for prokaryotes to ultimately spawn eukaryotes, they first had to go through a radical re-design of cell structure.

So here is what we have.  Prokaryotic cells can be viewed as the highest expression of mutation and selection, for there is no better cellular candidate for a “self-replicator.”  Yet after billions of years, the prokaryotic cell plan has failed to achieve anything near the level of structural complexity as exhibited by the eukaryotic cell plan.  To reach such structural complexity, the cell design had to be radically retooled, partly through endosymbiotic union, a one-time event given the widely accepted monophyly of eukaryotes.  Once the eukaryotic cell design was established, prior to the radiation of all extant eukaryotes, the basic cell design was now capable of supporting the emergence of complex, metazoan life.  The evolution of metazoa did not require further extensive retooling of the eukaryotic cell plan, given that metazoan cells are so similar to protozoan cells; it was more like the natural outflow of the potential inherent in the eukaryotic cell plan.

It turns out there is now more scientific evidence to support the contention that the emergence of the eukaryotic cell plan was a necessary prerequisite for the emergence of something as complex as a mouse:

Classic Cell Animation

You have probably seen the 3 minutes version, but I just found out that the complete 8 minute version is on youtube:

Also, the narrated version is below the fold:

Make them grow!

There is a way to inoculate a culture of media with just a few dozen cells of Tetrahymena and get it to grow into a flourishing population.  Consider the figure below (from [1]).  In panel A, you see the phenomenon I spoke of in the last entry, where a culture that starts with less than 500 cells/ml dies, but flourishes when started with 5000 cells/ml.  Yet in panel B, you can see this density-dependence is gone.

What happened?  Something was added to the cultures shown in panel B.

The Pack

I previously offered a puzzle to think about:

You are given two flasks, A and B, each filled with a 10 mls of a solution that contains all the nutrients needed for Tetrahymena to survive and grow.

On Friday, you are given a tube that is filled with thriving Tetrahymena and transfer 10,000 of these cells to flask A. Drawing from the same tube, you then add 1,000 cells to flask B.  You go home and celebrate Easter, returning to the lab on Monday.  You find the cells in flask A to be thriving, having spawned millions of new cells.  But when you look at flask B,  the cells have not grown and divided.  On the contrary, they all died!

Why did the cells in flask B all die in a sea of food?

The only difference between the two flasks if the density of cells.  Flask A starts with 10,000 cells in 10 mls, thus it has a density of 1000 cells/ml.  Flask B has a density of 100 cells per ml.  Why is this significant?

If we think in terms of front-loading, perhaps we should look to complex, metazoan features to explain this protozoan phenomenon.  And sure enough, this density-dependent survival is also well known among scientists who culture mammalian cells.  In other words, if you take a few human cells and put them into a Petri dish with lots of nutrients, those cells will also die instead of developing into a massive population of cells.  So why is this?

Cell Plans and Evolution

As I noted in the previous entry, Steve Matheson does not see eye-to-eye with me regarding introns and design.  In fact, he lists several areas of significant disagreement.  Let’s have a look.

Follow the Light

Watch three different fibroblasts (connective tissue cells) reach for pulses of near- infrared light:

Exquisitely Organized

In The Design Matrix, I documented how scientists originally envisioned the cell as an entity that was not very sophisticated or organized.  Yet this original “prediction” did not turn out to be correct.  In fact, a month or so ago a review article was published in the journal Science which continues to illustrate my point:

Bacteria were once viewed as amorphous reaction vessels with chromosomes that wandered freely and randomly throughout the cell.  The advent of genetically encoded fluorescent reporters harnessed to powerful cell-imaging technologies has enabled in vivo tracking of protein movement and revealed a strikingly complex inner world within bacteria.  This inner environment is exquisitely organized, in a highly controlled state of flux, and responsive to changing functions demanded of the cell.  – Shapiro, L., McAdams, HH, and Losick, R.  2009. Why and how bacteria localize proteins.  Science 326: 1225-1228.

In The Design Matrix, I drew out the significance of this:

Smart and Smarter

One of the expectations from the hypothesis of front-loading evolution is that cells would play a significant role in their own evolution, as this would constitute an intrinsic factor to evolution that would be more strongly connected to the original design event.  To this end, consider just how smart cells can be:

Scientists studying how bacteria under stress collectively weigh and initiate different survival strategies say they have gained new insights into how humans make strategic decisions that affect their health, wealth and the fate of others in society.

[…]

“We have developed for the first time a system level model of a large gene network to decipher the underlying principles of the bacteria game theory and how an internal network of genes and proteins is used to calculate risks in this complicated situation,” he said.

This has applications to human society because many people encounter similar dilemmas during their own lives. For example, should people ignore side effects and vaccinate against a new potentially lethal virus or should they not vaccinate and take the risk of being infected with the possible consequences? If the majority of the population is going to get vaccinated, then it is better for each individual not to get vaccinated. However, if most people will not be vaccinated then it is better to be vaccinated.

“What each bacterium is doing is the equivalent if each individual on earth was able receive the exact information about the rate of spread of this new virus, the exact information about the intensions, to be vaccinated or not, by each person on the planet, and in addition the exact information about the health risks of side effects or being infected,” said Ben Jacob. “A decision is then made in the context of this vast amount of information.”

“We have shown how the bacteria do this complex calculation according to well-defined principles,” added Onuchic. “We learned a simple rule: Anyone who needs to make a decision under pressure in life, especially if it is a possible death decision, will take its time. She or he will review the trends of change, will render all possible chances and risks, and only then react.”

And speaking of humans, consider this research: