🚀 go-pugleaf

In article <robison1.724623436@husc10> robison1@husc10.harvard.edu (Keith Robison) writes:
>adpeters@sunflower.bio.indiana.edu (Andy Peters) writes:
>
>>As for parasites leading to speciation, I suppose it depends on how
>>you define "species" in the case of asexual organisms.  The definition
>>above seems to be, "any new genotype."  Mind you, I am what W. D.
>>Hamilton has referred to as a "host-parasite coevolution freak"
>>myself, and I'm glad when anything can be explained in terms of
>>parasites :-), but it doesn't seem like any sort of new mechanism has
>>been offered here; since "incompatibility" means nothing in an asexual
>>population, there's no need for it here.
>
>Of course, many species in this world don't fall neatly into 
>"sexual" and "asexual", and perhaps it's in that realm where these
>effects might be most relevant.

>>>What about for sexual species?  Well, the same should apply IF
>>>the "dodges" used by different variants affect the fitness of
>>>hybrids between those variants, such as changes in reproductive
>>>structures (macro or micro), alterations in the timing of reproduction,
>>>gross genetic rearrangements, etc.  
>
>>Here's where "incompatibility" is more likely to become important.  I
>>would argue, however, that any "revolutionary" strategy for avoiding
>>parasitism (or any other strong selective pressure) would spread
>>rapidly through a sexual population, and not cause speciation unless
>>there was significant population subdivision.  If population
>>subdivision was being assumed, I apologize for reinventing the wheel.
>
>>>Keith Robison
>>>robison@biosun.harvard.edu 
>>-- 
>>--Andy
>
>Again, this phenomenon of selection-driven sympatric speciation would require
>the following conditions:
>
>	(1) Multiple possible beneficial adaptations ("dodges")
>	(2) The different adaptations are either 
>	    a. inherently incompatible
>	    b. reduced fitness of hybrids
>
>Imagine the following scenario:  suppose you have an organism (A) which
>generally reproduces asexually but occasionally uses sexual reproduction.
>Suppose further that another species (B) begins preying on the first,
>using the sexual apparatus as it's route of attack.  A situation such
>as this exists in E.coli, whose F (sex) pilus is also the receptor
>for filamentous phages such as M13.  There might be multiple alterations
>of A's sexual apparatus which might reduce predation by B.  However,
>these alterations may also hinder the ability of an altered A to mate
>with other A's bearing different modifications.  Alternatively, some
>B may mutate so that they can prey on particular modifications of A, but
>do this by trading off their ability to prey on the wild-type A.
>Here is a summary:
>
>			mates with    attacked by
>wild-type	A	   A		B
>		A1	   A1		B1
>		A2	   A2	 	B2
>
>
>If this were the case, then it would definitely be disadvantageous
>to acquire an A1-A2 phenotype, because then both B1 and B2 would be
>predators.  

This mechanism would certainly work if all the assumptions were met.
Are there really multiple "dodges?"  Is it safe to assume that an
A1-A2 phenotype would be susceptible to both B1 and B2; if they're two
modifications of the same feature, mightn't crossing lead to a third
modification?  Most importantly, is there any reason to expect _both_
strategy A1 and strategy A2 to arise at about the same time?  If, say,
only A1 arises, it will spread through the population on its own,
completely replacing A; only if two novel strategies arise at the same
time can I see this mechanism working.  Don't get me wrong, the
mechanism seems viable, given the assumptions.  I just wonder how
often the conditions are met in the real world.

>Keith Robison
>robison@biosun.harvard.edu 


-- 
--Andy
     "God is a real estate developer / with offices around the nation
          They say one day he'll liquidate / his holdings on High
             I say it's all speculation." -- Michelle Shocked