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- The molecular basis of transdifferentiation

Transdifferentiation is defined as an irreversible switch in postnatal life of one type of already differentiated cell to another type of normal differentiated cell [1]. Normally dedifferentiation and cell division are essential intermediate processes although they may not be obligatory in all cases [2]. Transdifferentiation belongs to a wider class of cell type conversions referred to as 'metaplasias'. By definition, metaplasia is the general name used to describe the conversion of one cell or tissue type to another. Under the definition of metaplasia, stem cells of one tissue type can switch to become those of another [3]. Transdifferentiation and metaplasia are associated with a discrete change in cellular morphology associated with a change in the programme of gene expression. At the molecular level, the cause of transdifferentiation is presumably a change in the expression of a master regulatory (master switch) gene whose normal function is to distinguish the two tissues in normal development [1, 3]. During embryogenesis, different tissue types arise from a common cell sheet because different combinations of master switch genes are switched on in each region in response to inductive signals. Since transdifferentiation appears to be the result of a single-step change, it is logical to assume that tissues between which such changes occur are neighbours in the sense that the combination of selector genes that defines them differ only in the state of one gene. Where the new tissue normally consists of more than one cell type, formed from a common stem cell, the metaplastic foci usually contain all these cell types. This indicates that metaplasia represents a switch of state from one stem cell to another. In the present review we shall discuss the identification of selector, or master switch, genes as well as examples of transdifferentiation in which the molecular basis is at least partly understood.

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