🚀 go-pugleaf

toms@kaylor.ncifcrf.gov (Tom Schneider) wrote:

>Ken Muldrew (kmuldrew@acs.ucalgary.ca) wrote:

>: (I seem to be suffering now from the same sort of
>: confusion that I get when I think about 'communication' theory and
>: 'information' theory--I suppose what I really need is to learn more
>: about both rather than dwell on my confusion about the difference).

>My understanding is that "communication theory" is the name Shannon originally
>used but that it was realized by people that the same mathematics applies to
>many systems and so is now called "information theory".  Does anyone else have
>an idea about this?  On page 173 of Shannon1993 (as listed in the faq) he seems
>to use the two interchangeably.

The do seem to be interchangeable in the few tidbits that I've looked
at. I was really using those words in a less technical sense in which
'communication' only concerns transmission of information (ie. you can
assume that the recipient understands English, or math, or whatever)
and information refers to the less well-defined case in which you
can't make those assumptions (I'm thinking about algorithmic
information, but I don't think I stated that too well).

>: The information as to where to
>: cut and splice these sequences has to be coded somewhere and the
>: introns just happen to be at the right place at the right time. Since
>: RNA is single stranded, it can (and probably does) fold in on itself
>: to form hydrogen bonds. The introns probably contain sequences which
>: allow for specific tertiary structures to form which are then
>: recognized by splicing proteins (look at a picture of a tRNA to get an
>: idea of what I'm talking about here).

>Although you are right that there are structures, I think that the majority
>of the sequence conservation for locating the boundaries between introns
>and exons is simple pattern in the sequence.  See:

>  http://www-lmmb.ncifcrf.gov/~toms/paper/splice

>(especially pages 31 and 32) for a detailed information analysis.

Yes, I just had a nice picture pop into my head and typed without
giving it enough thought; it's been many years since I studied any of
this.

>: Another idea is that the DNA replication machinery was built to handle
>: genomes which are much smaller than in eukaryotic organisms. Thus the
>: error rate which was built into the system (it's the same machinery
>: for all living things) was designed to introduce novelty at a rate
>: which was consistent with a smaller genome. There will be a certain
>: critical size for the genome, beyond which, the errors introduced by
>: copying will corrupt the genome too quickly (ie. there will be too
>: many errors introduced into the genome to make a viable offspring).
>: Thus the non-coding DNA is there to absorb mutations. If a point
>: mutation occurs every 10^9 bases (I think the copying errors are about
>: 1 in 10^6, but there are proof-reading enzymes which improve this),
>: then you spread your gene out so that maybe you only get half the
>: mutation rate within the coding region.

>Shannon's channel capacity theorem says that the copying error can be made
>small enough to be tolerable.  See:

>  http://www-lmmb.ncifcrf.gov/~toms/paper/ccmm
>  http://www-lmmb.ncifcrf.gov/~toms/paper/nano2

>In the famous little book:

>@book{Schroedinger1947,
>author = "E. Schroedinger",
>title = "What is life? the physical aspect of the living cell
>\& Mind and matter.",
>publisher = "Cambridge University Press",
>address = "Cambridge",
>year = "1947"}

>I seem to recall that Schroedinger did some calculations about the target size
>of DNA for radiation.  The point is that you can't "hide" because if you
>increase the total genomic size, the important genes are still going to be hit
>at the same rate because they still present the same physical cross section to
>radiation.  Also, the polymerase won't make fewer mistakes in one place just
>because it (or an entirely different molecule) also has to function at another,
>as this may be mostly from thermal noise, which is everywhwere.  Further,
>increasing the size increases the likelyhood of generating binding sites that
>sop up proteins from where they are needed.  (The system can eventually evolve
>to get rid of many if not most, but the probability of them coming up randomly
>is increased.)  Finally, increased size increases the likelyhood of damage to
>the long fragile molecule.

OK, the coding region presents the same cross-section, no doubt about
that. I had an uneasy feeling when I was typing in that bit. I think
that what you typed here supports the idea that this DNA isn't simply
"junk"--a lot of energy goes into taking care of these long, fragile
molecules. Just to give people an idea of how fragile DNA can be, a
caucasian without sunscreen, standing in the noon-day sun of the
tropics, will suffer about 50 000 single strand breaks in every skin
cell that's exposed per hour (just about the maximal rate of repair,
coincidence?).

Another purpose for introns may be to signal the DNA repair or
proof-reading enzymes to stop. I think that point mutations have
accrued in the hypervariable regions of immunoglobulin genes at a rate
that is higher than the replication error rate, implying that there is
a mechanism to promote mutation. If there was a sequence which told
the proof-reading enzymes to stop when they reached that particular
region, then that might be a way of generating the higher mutation
rate. 

Ken Muldrew
kmuldrew@acs.ucalgary.ca