Mechanisms Causing Somaclonal Variation
The Somaclonal variation may be attributes to i) pre-existing variation in the somatic cells of the explant or ii) Variation generated during tissue culture ( epigenetic) often both factors may contribute.
The original Ploidy level of the plant or plant organ from which the explant is taken may play an important role in Somaclonal variation. Meristematic explants such as apical meristem derived from either shoot apex or axillary bud, have a lesser degree of genetic variability as compared to plants regenerated from non-meristematic explants which generally produce genetic variability. Cells of meristematic explant divide by normal mitosis and cells are maintained at a uniform diploid level. However, the cells in non-meristematic explants are derivation of the meristematic part of the plant and during their subsequent differentiation, do not divide by normal mitosis, but undergo DNA duplication and end reduplication. Endo reduplication leads to the formation of chromosomes with four chromatids, chromosomes with eight chromatids and polytene condition.
When the cells of various genomic constitutions of the initial explants are induced to divide in cultures, the cells may exhibit changes in chromosome number such as aneuploids and polyploids. Organogenesis and or embryogenesis occur mostly from diploid cells. Therefore, pre-existing variation in explant tissue always rule out the Somaclonal variation in the culture. The presence of several chromosomal aberrations such as reciprocal translocation, deletion, inversion, chromosome, reunion, multicentric, acentric fragments, Heteromorphic pairing etc were found among the somaclones of barley, ryegrass, garlic and oat. Besides these changes, there are examples of phenotypic variation which can be observed in plants regenerated from cultured cells or protoplasts variation which can be observed in plants regenerated from cultured cells or protoplasts where no apparent chromosomal abnormalitites are seen.