The Marcus Rhoades Experiment for Dummies (like me)

One of the things I learnt during this past year at a certain local university was that advanced biologists the world over can't teach for nuts.

There is some information on the Marcus Rhoades Experiment online. The best account is here. It assumes you already have a phD-level understanding of the subject.
It was obvious to me that our uni lecturer ripped his slides from here - however he didn't have the requisite phd-level understanding. In fact he completely got it completely wrong - and attributed "what was causing the dotted phenotype?" to spontaneous mutation in somatic cells, although the next line in the text "A reverse mutation of a1 → A1 in somatic cells would be an obvious possibility, but the large numbers of dots in the Dotted kernels would require extremely high reversion rates" makes it quite clear why Marcus Rhoades refused to believe this. I think it's almost criminal that a university lecturer could teach his flock completely the wrong thing because he couldn't be bothered to take the time to find the truth. I found the truth by thinking really, really hard about it. Sadly it didn't come out in the exam.

fig 1 - the offending slides

So now that I've got a little bit of time, I'd like to explain the experiment as clearly as I can for any future generations of "advanced biologists" out there who have to suffer the same incompetent teaching that I did. (It will help to read the immuneweb pdf immediately AFTER this.)

Marcus Rhoades was some guy who liked corn. Specifically Mexican Corn. A lot.
He liked it so much he bred it at home in his spare time, and took note of what colour the kiddy corns turned out. This is the kind of thing people did before the Internet was invented.

Mexican Corn is special - the ears can look yellow, like the type you'd eat, or all-black (yes, like the kiwis) like the type only Mexicans would eat.

The black variety is dominant.

So like all bored geneticists, Rhoades entertained himself with intellectual masturbation by naming A1 the dominant allele for pigment (ie black), and a1 the recessive allele for no pigment (ie colourless, ie normal looking corn.)

He took true breeding black corn (true breeding means you cross with the same genotype, and it keeps making the same phenotype) ie homozygous A1A1 and crossed it with itself.
(Who knows. Maybe he was trying to make devilspawn-corn)
He wound up with a dihybrid ratio. Now if he'd just had pigmented and colourless, you'd peg it to a mistake -- A1/a1 instead of A1/A1, ie non true breeding parents.

What he got was a modified mendelian dihybrid ratio of 12:3:1 for pigmented (black) : dotted : colorless. (dotted = ear has mix of black and normal coloured kernals. like sweet and salty mixed popcorn. kinda.)

So he sat back and thought... whoa. DOTTED? what the f***? (A normal person like you and I would just have eaten the damned corn. And thrown away the black bits.)

So he envisioned a new allele, Dt for dotted, and dt for... not dotted, reasoning that his observations must have been the result of 2 separate events occurring at 2 unlinked (ie not immediately adjacent to each other, so independent) sites:

1) A1 reverting to a1 (to produce the colorless kids, a1a1)
and
2) dt changing to Dt (to make dots where before there were just kiwis. I mean all-blacks. Dt only works when there is a1a1 -- then it makes dots. When there is A1/- (ie A1/anything, eg A1/A1, A1/a1... then all you see is kiwis. No dots. Regardless of whether Dt or dt.)

(confirmed by genetic analysis)

He asked himself "but wait, how is this even possible?"
"I mean, if we have a1/a1... then how the #%@ can Dt/- (the presence of at least one dominant dotty allele) have any effect? There's no pigment being coded for at all! (ie no A1)"

Obviously things were more complicated than they seemed. There MUST be A1 hanging around somewhere in the background, in our presumably a1/a1 plants. This would be explained by a mutation happening after the analysis (which for all intents happens when the baby plants are still little seedies. the analysis that is.)

Then he asked, "what is CAUSING the dots?"
"maybe... if I have a totally colourless (ie yellow looking, ie a1a1) corn and some of the SOMATIC (non sex) cells mutate spontaneously to A1... then I can wind up with a couple black dots... holding the ear in his hands and looking at the thousand or so dots, he then thought "naaaaaaaaaaaaaah." After all the odds of this happening are about as low as the PAP losing the next GE.

So genius corneticist that he was, he presumably ate the corn. Next he took boy-plants KNOWN to be a1/a1, Dt/- (ie the Dotty guys) and looked at their anthers, presumably with a microscope. He took pollen grains and fertilized known a1/a1 females, and lo and behold, some of the progeny were ALL BLACKS.

Meaning the mutation (a1 to A1) in the boy plants that he KNEW were a1 (ie the mutation happened after, or outside his genetic analysis) was in their GERM cells (NOT SOMATIC) and transmissable to the next generation, and it could turn dottys into all blacks. Heavy stuff.

Most of us would have given up by now and gone for a pint. But Rhoades, being made of sterner stuff (or maybe he had no friends to go for a pint with) thought about it some more, and more, and more, and then it hit him...

... it could be explained in terms of "instability".

These mutations from a1 to A1 were a result of some kind of genetic instability.
He noticed that this instability never occurred, unless there was Dt present.
(ie a1a1/dtdt never turned into all blacks out of the blue)
However, when Dt was present, a1/a1 became fairly unstable, and black kids tended to appear. (Oh, the scandal.)
Conversely, when he crossed the new all-black pigmented progeny to breed OUT the Dt, he never wound up with unpigmented offspring. (A1 doesn't go away.) -- this was just his control arm. Not important to understand this.

So maybe... the presence of Dt was causing the instability.

Here's where the genius comes in:

Rhoades proposed a mechanism for the instability -- the inheritence of a mutation caused by a defective transposon.

Think of the transposon (a transposable piece of DNA) as a promiscuous gene who really wants to move from one partner to the next. Only it can't move unless the "Dt" transfactor (not the boyfriend-to-be, but some other... interrim guy who emboldens the transposon to jump ship...) is present as well -- because the Dt transfactor accidentally makes the gene products that enable the transposon to move.
When the conditions are right, off flies the transposon down the genome, to a1 where it bumps out one a1, and turns into A1, effectively stealing his/her girlfriend/boyfriend.

However without Dt around, the A1 transposon remains stable, or faithful, because she/he has no reason to move on.

Tadah. There you have it. The Marcus Rhoades Experiment.