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Chitinases have been identified in a variety of organisms ranging from prokaryotes to eukaryotes, known to specifically degrade chitin, an abundant polymer of N-acetylglucosamine. Recently a human chitinolytic enzyme called CHIT1 was discovered. CHIT1 is expressed by activated macrophages and hydrolyzes artificial chitotrioside substrates, but its specific function in humans is unknown, since it is generally believed that man completely lacks endogenous chitin and endogenous substrates for chitinases. An intriguing question is whether the chitotriosidase activity is just an evolutionary remnant or it has a physiological function in man. To test these hypotheses we utilized a “phylogenomic” approach performing accurate sequence analyses of this gene, coding for CHIT1, in rodents and primates. Inspecting the sequences available in public databases, we determined that this gene is conserved in rodents (mouse and rat) and primates (chimpanzee, gorilla, orangutan, gibbon, baboon, a common marmoset and black macaque). Moreover we found that a 24-base pair duplication that determines an enzymatically inactive human protein is not present in primates, suggesting that this polymorphism was created during human evolution. These results indicate that chitotriosidase is conserved across the evolutionary scale. Such conservation of the CHIT1 gene argues in favour of an important biological role. Copyright © 2003 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

The genomes of most organisms contain multiple copies of genes that are closely related in structure and function. Such gene families can arise from tandem duplications, as in the case of the HOX clusters, or from ancient polyploidization events which occurred in primitive chordates. The reason why multiple copies of an intact gene in a particular genome are preserved is unclear although an increase of protein level may provide a selective advantage to the organism, maintaining extra copies in subsequent generations.

The article reveals the molecular cloning and fine mapping of API5L1, a novel human gene strongly related to an antiapoptotic gene. Apoptosis or programmed cell death is a physiological form of cell death that occurs in embryonic development and organ formation. It is characterized by biochemical and morphological changes such as DNA fragmentation and cell volume shrinkage. It occurs after the removal of extracellular growth factors or cytokines, thus the cell viability is dependent on the balance between the factors that favor apoptosis and those signals which favor survival.