The classic model organism was E. coli (in fact, just certain genetic strains of E. coli.) & T-2 and T-4 bacteriophages
Hundreds or even thousands of scientists concentrate their research on just one species, discovering how that organism works in detail
The following are examples of species on which research is systematically concentrated today:
Drosophila menanogaster (fruit fly)
Mus musculus (common mouse)
Saccharomyces cerevisiae (yeast)
Caenorhabditis elegans (a tiny nematode worm)
Arabidopsis thaliana (a small higher plant)
Zebra fish (just like the ones in the pet store!)
Dictyostelium discoideum (a small amoeba)
Chlamydomonas reinhardtii (a one celled alga / plant)
(related to Volvox and Pandorina, which are multicellular)
& there are dozens of other "model organisms"!
What makes a good model organism?
NOT that it is inherently important,
Not necessarily useful (though corn and rice are model organisms)
Can reproduce in the lab (nearly impossible with sea urchins)
Short reproductive cycle (frogs are a problem)
Small genome (not too much junk DNA, not polyploid)
Not cute (so PETA won't hate you, or your own kids)
The genome of each model organism is being sequenced
Special books are written for each model organism
concentrating all available knowledge about it.
NSF (etc.) funds national stock centers for each model organism
the zebra fish center is at U of Oregon
UVA has a frog center
the Chlamydomonas center is at Duke
Stock centers collect and maintain genetic mutant strains (100s or thousands!)
They send out cultures of mutants to scientists who order them.
(or sometimes to high school students doing science projects!)
What can you learn from mutants of model organisms?
Each mutant has 1 particular protein that is abnormal or missing because the gene encoding it has been altered
By comparing mutants, scientists test theories about basic biological mechanisms.
For example, mouse mutations that cause various birth defects
are used to find molecular explanations for human birth defects.
Suppose scientists find 123 different loci in the genome where mutations cause abnormalities in mouse gastrulation,
then that implies 123 different proteins are used in gastrulation.
The functions of each protein can be figured out from the specific effects of mutations in that gene,
and often also from the base sequence, from which the amino acid sequence can be deduced,
and computers used to compare it with data bases.
Suppose mutations in a gene cause abnormalities in gastrulation
and the gene codes for a protein whose amino acid sequence is similar to a cell surface receptor found in amoebae (or anything),
then probably that gene codes also codes for a receptor protein.
If this amoeba receptor served to bind to a certain other protein, then one could look for similar signal proteins in the mouse.
Most of the molecular mechanisms described in our textbook were discovered, at least in part, by this approach.
Lethal mutations are more difficult to study, unless recessive.
Even dominant lethal mutations can be studied if you find temperature-sensitive mutations,
in which the protein is abnormal only at temperatures above a certain threshold.
Nevertheless, it is important to notice that genetic screens tend to miss whatever genes are the most important, if even small changes prevent survival of the organism.
(this is the Achilles Heel of genetic analysis; & you can appear very wise at a research seminar, by asking "Have you considered whether the key mutations may be lethal?")
Mutations affecting flagella and photosynthesis are among the most important in Chlamydomonas.
They can survive without being able to swim, and be fed by external carbon sources. (other plants die without photosynthesis
and Paramecia, etc. would starve if their cilia were paralysed.)
The life cycle of Chlamydomonas is interesting but odd.
Instead of two sexes, they have two mating types
called plus and minus (but not because of electric charge!)
Imagine if human eggs and sperm had the same size & shape,
or men & women were morphologically the same, but breeding required one of each of two kinds,
like maybe if Republicans could only marry Democrats, but they looked the same,
or IBM people could only marry Mac people,
or UNC people only Duke people (stop this analogy!)
Key points about the Chlamydomonas life cycle:
-- Plus and minus cells recognize each other by proteins on their flagella
-- The flagella stick to each other, bringing the anterior ends of the cell bodies together
-- A cytoplasmic bridge forms between the two cells
-- The cells then fuse to form a diploid zygote
-- A hard wall is formed to create a zygospore that can withstand drought and extreme temperatures
-- When environmental conditions improve, the zygote undergoes meiosis and germinates to release four haploid cells.
Two of these haploid cells will be mating type plus and two will be minus, because mating type is controlled by a single gene.
The multicellular alga Volvox is genetically very close to Chlamydomonas.
About 500 species of Chlamydomonas have been named based just on what you can see in a light microscope.
DNA sequencing shows that they diverged into several different branches far back in evolutionary time.
Multicellular forms (Gonium, Pandorina, Volvox) evolved in at least 3 of these branches.
The species of Chlamydomonas that is used as a model organism is closely related to one particular species of Volvox, much more closely than it is related to some other species of Chlamydomonas.
Note: Volvox is not the direct ancestor of higher plants (which evolved from some other kinds of green algae).
Take-home message: Multicellularity has evolved many times.