Organisms of different species have different shapes and sizes and still, within the same species, shape and size are practically constant. For example, elephants can be 250,000 larger in volume than mice, yet when we compare elephants of the same species and controlling for age they shouldn’t differ by more than 2x (I’m is guessing – I couldn’t find any reference for this). How do organisms within a species maintain relatively constant shapes and sizes when it’s at least physically possible to have wide variations?
This seems a question for developmental biologists, but microbial cell biologists are very interested in their version of the same problem. Bacterial species can vary enormously in cell shape and size. One of the largest, Thiomargarita namibiensis (100–300 µm), can be 1000x longer than one of the smallest known Mycoplasma genitalium (~300 nm). Nonetheless, within a species, their sizes are often constant and, we imply, very well regulated. There was a recent burst of papers where different groups across the US measured with unprecedented precision the distribution of cell lengths in the rod shaped bacteria E. coli, Calaubacter crescentus and Bacilus subtilis. From this collective work a simple mechanism seems to emerge: Rod shaped bacteria decide when to divide by determing that they added a fixed increment to their cell length. This so called “incremental rule” (a.k.a. “adder model” or “constant size extension“) had been proposed earlier but lacked empirical support. It provides a simple explanation for why cell populations maintain a narrow size distribution – I strongly reccomend reading those papers.
We added additional evidence for the incremental model by showing that the pathogen Pseudomonas aeruginosa, our model organism, also follows the incremental rule. Our interest in this problem came by accident when we isolated a mutant with abnormally long cell from our hyperswarming experiment. In our new paper we analyze the length distribution in wild-type Pseudomonas aeruginosa and in this mutant which we call frik, not only because it is a freak but also because it reminds us of the tasty dutch snack frinkandel.
The frikandel is a meat based rod of mysterious composition. It’s probably made with left over meat, but it’s hard to tell exactly what its composition is from it’s spicy taste and spongy texture (hmmm…). Similarly, exactly why the frik cell is abnormally shaped is somewhat a mystery to us. We resequenced the genome of the frik mutant and we found two candidate mutations. We were capable of ruling out one of those two using microbial genetics. The second one, however, is really hard to clone and we could not confirm nor refute that it is the cause of the frik phenotype. One explanation is that the mutation is in a gene (PA14_65570) that may be essential which would make it harder to clone.
Still, our paper extends the reach of the elegant incremental model by showing that it also applies to P. aeruginosa, a common cause of opportunistic infections. We also show that the frik cells are more sensitive to some antibiotics, suggesting that affecting cell size regulation could have implications for improved antimicrobial therapy.
Read our paper:
Cell size homeostasis and the incremental rule in a bacterial pathogen
Maxime Deforet*, Dave van Ditmarsch* and João B. Xavier. Biophysical Journal