Abstract

Vegetative plant propagation may lead to heritable phenotypic changes, a phenomenon known as somaclonal variation. The underlying molecular causes relay in the breakdown of a preexisting chimerism, or in the induction by stress of rather controlled chromatin remodeling at epigenomic and genomic levels, as well as in less extent mutations, generally considered to occur randomly. The controlled epigenetic alterations may facilitate subsequent concrete genome reorganizations and, both together, the occurrence of other DNA sequence mutations in genomic regions constitutively more labile or that become more exposed. Thus, chromatin remodeling, as a plastic response of plant to manage stress, is a controlled effect that may facilitate specific genome changes probably not so random. This should result in more frequent variant phenotypes (somaclones), such as the dwarf types of banana and plantain generated after several cycles of micropropagation. Several studies pointed out that the banana (epi)genome might became unstable during increased multiplication cycles, resulting in higher somaclone indexes. The most applied plant growth regulator for banana micropropagation is the cytokinin 6-benzylaminopurine, which promotes the development of new shoots, another possible defense response of plant to the specific stress generated by the whole set of artificial culture conditions. The contents of such molecule and its metabolism in the plant along subcultures affect both organogenesis and somaclonal variation by inducing chromatin changes that affect developmental processes and phenotype, respectively. In the present chapter, we express our opinion about these facts on the bases of reviewed literature and our own experience.

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