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The development of a single cell into a large, complex organism with well-organized tissues is an elaborate process requiring intricate regulation.  Cells have to divide, migrate, apoptos, differentiate, and undergo a host of other processes with clockwork precision in close coordination with other cells.  A defect in early development is universally lethal to a complex organism; similarly, even defects late in development are often profoundly detrimental to an organism's ability to survive in its environment.
 
The development of a single cell into a large, complex organism with well-organized tissues is an elaborate process requiring intricate regulation.  Cells have to divide, migrate, apoptos, differentiate, and undergo a host of other processes with clockwork precision in close coordination with other cells.  A defect in early development is universally lethal to a complex organism; similarly, even defects late in development are often profoundly detrimental to an organism's ability to survive in its environment.
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These simple observations posed a significant paradox in evolutionary thought.  If evolution is driven by the force of natural selection acting on phenotypic variations between individuals, then how do these variations arise without irreversably disrupting intricate developmental processes?  The answer to this question is deceptively simple; these variations arise by reorganizing existing developmental processes while leaving their machinery (that is, [[genes]] and molecular signalling pathways) largely intact.<ref>http://www.tcd.ie/Biology_Teaching_Centre/assets/pdf/by2204/amclby2204/amclby2204-carroll-evodevo.paper.pdf</ref><ref>http://ww.explorelifeonearth.org/cursos/Bolker2000.pdf</ref><ref>http://www.biol.uw.edu.pl/empseb2010/images/artPigliucci1.pdf</ref>
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These simple observations posed a significant paradox in evolutionary thought.  If evolution is driven by the force of natural selection acting on phenotypic variations between individuals, then how do these variations arise without irreversibly disrupting intricate developmental processes?  The answer to this question is deceptively simple; these variations arise by reorganizing existing developmental processes while leaving their machinery (that is, [[genes]] and molecular signalling pathways) largely intact.<ref>http://www.tcd.ie/Biology_Teaching_Centre/assets/pdf/by2204/amclby2204/amclby2204-carroll-evodevo.paper.pdf</ref><ref>http://ww.explorelifeonearth.org/cursos/Bolker2000.pdf</ref><ref>http://www.biol.uw.edu.pl/empseb2010/images/artPigliucci1.pdf</ref>
    
The evidence for this explanation is abundant.  The genes responsible for regulating embryogenesis are very highly conserved among animals; they do not change significantly in sequence or function, even between clades that appear to be relatively distantly related.  For instance, the ''Hox genes'' (which are needed to organize body plan) are expressed in an almost identical pattern in a fruit fly embryo that they are in a mouse (or human) embryo.  The differences in developmental regulation that do exist between clades tend to be simple variations in the expression pattern of molecular developmental regulators, rather than structural variations in the regulators themselves.<ref>http://www.sinauer.com/gilbert9e/sample/Gilbert9e_Ch02.pdf</ref><ref>http://www.springerlink.com/content/a31n1412g741k03p/</ref>
 
The evidence for this explanation is abundant.  The genes responsible for regulating embryogenesis are very highly conserved among animals; they do not change significantly in sequence or function, even between clades that appear to be relatively distantly related.  For instance, the ''Hox genes'' (which are needed to organize body plan) are expressed in an almost identical pattern in a fruit fly embryo that they are in a mouse (or human) embryo.  The differences in developmental regulation that do exist between clades tend to be simple variations in the expression pattern of molecular developmental regulators, rather than structural variations in the regulators themselves.<ref>http://www.sinauer.com/gilbert9e/sample/Gilbert9e_Ch02.pdf</ref><ref>http://www.springerlink.com/content/a31n1412g741k03p/</ref>
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