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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its introns, as it turned out), Professor E. B. Lewis of Caltech was able to produce flies in which the halteres had been replaced by a second pair of wings.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: encode transcription factors each with a DNA-binding homeodomain 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. 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 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.