Plants tolerate polyploidy more readily than animals

[Toni Kazic]

Hi all,

I have heard no bad explanations that I can recall, so I will inflict one
upon you this quiet Friday evening (in my time zone).  I am terribly
underinformed and have not kept up, but here is a long shot . . .


It is certainly true that animals (and surely plants, but I don't know this
directly) produce *many* mutations which do not survive embryogenesis
and/or early life.  Approximately 1/3 - 1/2 of all human conceptions (sorry
I have forgotten which fraction) spontaneously abort prior to noticeable
onset of pregnancy (i.e. mom relatively unaware).  The general explanation,
which as far as I know is supported by the fragmentary studies permitted in
this country, is that the abortions are due to genetic abnormalities,
usually very significant (large or very sensitive translocations,
deletions, or inversions, aploidy of various types (I mean by aploidy a
non-diploid complement of loci, thus to include polysomies, polyploidies,
aneusomies, and aneuplodies.  I cannot at the moment recall the proper word
for this collection of states, or if one exists, so be forewarned if you
use it around your geneticist buddies.).  These show up as severe
developmental defects, presumably triggering the abortion.  There are of
course other developmental defects which are (by the crude methods of 20
years ago or incomplete RFLP mapping today, I imagine) cytogentically
normal, and which also induce spontaneous abortion, and of course the
environmentally-caused abortions.  I am personally always a bit staggered
when babies come out normal, but the selection is very severe so a fragile
process works.


It is worth pointing out that humans (and I guess other mammals) do
tolerate certain aneuploidies and polypoloidies --- XO, YO, XXX, XXY, XYY,
XXXX, XXXY are all found at low frequencies.  I don't have my ancient human
genetics text here at home so I can't describe the phenotypes, but in
general these individuals usually survive into adulthood, may be somewhat
fertile, and have some characteristic phenoypes.  I don't know about
ploidies for the autosomes, but I recollect that some have been observed.
Hyperploidies in mammals of the full haploid complement have not been
observed to the best of my inadequate knowledge (indeed, I would find it
very shocking).  Moreover human females are somatic mosaics of aneuploidy
in X (due to random inactivation of one of the two X chromosomes during
development).  So hyperploidy and aneuploidy are neither genetically nor
biochemically impossible in the general case.


Now the first question is what produces the complex phenotype of
spontaneous abortion (here restricting it to the chromosomally-related
cases).  In the case of aberrant ploidies and some somies, it is clear that
improper segregation of the chromosomes during mitosis is an important
factor.  In others, replication and segregation appear to carry on
normally, but the cells "sicken" or the developmental program (mmm, I
almost used the English/French spelling, Athel! ;-)) is "rechanneled" in
the Waddington sense of canalization.  I caution that I mean the verbs in
the previous sentence in both a statistical and a probabilistic sense ---
over the population of differentiating cells and within a given cell.


If we use the word metabolism broadly to include the entire biochemical
system, evolving within cells, through cell lineages, and in space, time,
and topology, then we have the basic problem of explaining phenotype in
terms of genotype and its evolving expression.  If a particular phenotype
is cell-autonomous (that is, not involving interaction with other cells), then
it seems to me that an analysis along the lines I suggested earlier (not
necesarily MCA or systems analysis, but some spiritual offshoot) may indeed
be a sufficent model for explanation.  In the case of non-cell-autonomous
systems, the model will be far more complex and obviously well outside the
scope of MCA, systems analysis, or this hypothetical offshoot.


And that's why it seems to me an enormously interesting question.
Admittedly we can't predict phenoypes well in cell-autonomous systems, even
very simple ones, so ones involving embryological folds, tissue migration
and apoptosis, trans-cell signalling, and evolving structures are even
hairier to formulate.  But hey, that's half the fun ;-)!



The second interesting question is why plants do better than animals.  When
I say "plasticity of the genome" I mean this both in terms of the
chromosomal mechanics and the resulting expressed biochemistry.  But the
underlying reasons for this tolerance are, as far as I know, unknown.  It
may be nothing less trivial than the mechanical properties of the plant
cells scale better with increasing size than those of animal cells.




Toni

p.s.  yes geneticists talk about these sorts of things, but over beer.
Fundamentally, the conceptual apparatus is limiting, so significant
improvements in the models will be terribly important.



Toni Kazic, Ph.D.
Institute for Biomedical Computing
Box 8036
Washington University
700 South Euclid Ave.
St. Louis MO  63110

314-362-3121  (vox)
314-362-0234  (fax)

toni at athe.wustl.edu
http://ibc.wustl.edu/~toni