Download (part of a “developmental reprogramming”). The roots of evolutionary

Evolutionary Developmental Biology (Evo-Devo) deals with
the relationships between the individual development and the
phenotypic changes of the organism during evolution. Major
morphological transitions in evolution are presently recognized
to be accommodated by a few key developmental genetic
changes (part of a “developmental reprogramming”). The roots
of evolutionary changes in animal shape and form can be identified by studying the
developmental mechanisms that control body pattern and shape in embryos. Evo-devo research
on how do novelties originate in evolution and where does the novelty come from?
Wallace Arthur (2004) notes that developmental novelties originate in four possible
ways: altered timing (heterochrony), altered positioning (heterotopy), altered amounts
(heterometry) and altered gene product (heterotypy).
1. Heterochrony-changing the time or duration of developmental phenomena or gene expression
2. Heterotopy-changing the placement of developmental phenomena or the cell types in which a
gene is expressed
3. Heterometry-changing the amount of gene expression in a manner sufficient to alter the
phenotype
4. Heterotypy-changing the sequence of the gene being expressed during development.
These mechanisms have profound significance for how new traits can be generated, how
they become integrated into developing organisms, and how they can become propagated
through a population. It is argued that adding these developmental data and contexts provides a
new and more complete theory of evolution, including a theory of body construction along with a
theory of change.
Heterotypy in the Ultrabithorax protein that specifies in insects. The insect body
plan consists of head, thorax, and abdomen. The thorax is built from three
segments, T1, T2, and T3. Each carries a pair of legs; hence insects are six-legged
creatures.
In most of the insect orders, T2 and T3 each carry a pair of wings (the honeybee is
an example). However, flies belong to the insect order diptera; they have only a single pair of
wings (on T2). The third thoracic segment, T3, carries instead a pair of balancing organs called
halteres.
In Drosophila, a gene called Ultrabithorax (Ubx) acts within the cells of T3 to suppress the
formation of wings. By creating a double mutation in the Ultrabithorax gene (in its introns, as it
turned out), Professor E. B. Lewis of Caltech was able to produce flies in which the halteres had
been replaced by a second pair of wings.
Ultrabithorax (Ubx) is an example of a "selector gene".
Selector genes are genes that regulate (turning on or off) the expression of other genes. Thus
selector genes act as "master switches" in development.
Wings and all their associated structures are complicated pieces of machinery. Nonetheless,
mutations in a single gene, were able to cause the reprogramming of the building of T3 (and
deprived the flies of their ability to fly).
Selector genes encode transcription factors. Ultrabithorax encodes a transcription factor that is
normally expressed at high levels in T3 (as well as in the first abdominal segment) of
Drosophila.
Most selector genes, including Antp and Ubx, are homeobox genes
Antp, Ubx, and a number of other selector genes have been cloned and sequenced. They all
contain within their coding regions a sequence of some 180 nucleotides called a homeobox. The
approximately 60 amino acids encoded by the homeobox are called a homeodomain. It mediates
DNA binding by these proteins. Many proteins containing homeodomains have been shown to be
transcription factors; probably they all are.
The table shows the sequence of 60 amino acids in the homeodomain of the protein encoded by
the Drosophila homeobox gene Antennapedia (Antp) compared with the homeodomain encoded
by the mouse gene HoxB7; by bicoid (bcd), another homeobox gene in Drosophila; by
goosecoid, a homeobox gene in Xenopus; and by mab-5, a homeobox gene in the roundworm
Caenorhabditis elegans. A dash indicates that the amino acid at that position is identical to the
one in the Antennapedia homeobox domain. [Link to the single-letter code for the amino acids.]
Note that the mouse homeobox in HoxB7 differs from the Antp homeobox by only two amino
acids (even though some 700 millions years have passed since these animals shared a common
ancestor). HoxB6, used in the experiment described in the next section, differs from Antp in only
4 amino acids.
The Hox Cluster
Antp and Ubx are two of 8 homeobox genes that are linked in a cluster on one Drosophila
chromosome. All of them:
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encode transcription factors
each with a DNA-binding homeodomain
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act in sequential zones of the embryo in the same order that they occur on the
chromosome!
The entire cluster is designated HOM-C with
o lab, Pb, Dfd, Scr, and Antp belonging to the ANT-C complex and
o Ubx, Abd-A, and Abd-B designated the BX-C complex.
All animals that have been examined have at least one Hox cluster. Their genes show strong
homology to the genes in Drosophila.
Mice and humans have 4 Hox clusters (a total of 39 genes in humans) located on four different
chromosomes.
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In mice: HoxA, HoxB (shown here), HoxC, HoxD
In humans: HOXA, HOXB, HOXC, HOXD
As in Drosophila, they act along the developing embryo in the same sequence that they occupy
on the chromosome.
All the genes in the mammalian Hox clusters show some sequence homology to each other
(especially in their homeobox) but very strong sequence homology to the equivalent genes in
Drosophila. HoxB7 differs from Antp at only two amino acids, HoxB6 at four.
In fact, when the mouse HoxB6 gene is inserted in Drosophila, it can substitute for
Antennapedia and produce legs in place of antennae just as mutant Antp genes do.
This fascinating result indicates clearly that
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these selector genes have retained, through millions of years of evolution, their function
of assigning particular positions in the embryo, but
the structures actually built depend on a different set of genes specific for a particular
species.