Somaclonal variation
This technique has been described in detail by Larkin and Scowcroft (1981) and
specifically in fruit crops by Hammerschlag (1992). It arises when plant explants are subjected to a tissue culture cycle. The cycle includes establishment of a dedifferentiated
cell or tissue culture under defined conditions and the subsequent
regeneration of plants. Variation at cellular level occurs either in cells before
explant excision or during the tissue culture cycle (Skirvin 1978; Jain 2001;
Remotti 1998; Rami and Raina 2000). The degree of variation depends on many
factors, including:
- the origin of the explant used (organ, age, genotype) (Murashige 1974;
D’Amato 1975; Barbier and Dulieu 1980)
- the time that cells or tissues are maintained in vitro (Barbier and Dulieu 1980)
- the time and intensity of the mutagenic agents used (Burk and Matzinger
1976)
Reduction of somaclonal variation is achieved by using appropriate culture
media and by shortening subculture intervals. Somaclonal variation can be 10,000
times higher than spontaneous mutation rates in whole plants (Larkin and Scowcroft
1981). Many phenotypic variations reported in the regenerated fruit crop plants
were extensively reviewed by Hammerschlag (1992). Important changes include
growth rate and reproductive apparatus modification (sterility, precocious flowering
and flower abnormalities, internodal length), and leaf (variegation, albino,
chlorotic, etc.), thornlessness, isoenzymatic activity changes, and increased salt
resistance, fruit colour, etc. An increased ploidy level has been reported in kiwi
subcultures (Rugini
et al. 2000b) and in grape (Kuksova
et al. 1997). Some changes
are not hereditable, since they have epigenetic origin. These changes include:
- cytokinin and auxin habituation (Meins and Binns 1977)
- chilling resistance (Dix and Street 1976)
- changing susceptibility to fungal attack (Potter 1980)
- susceptibility to certain pathogens, due maybe to virus elimination during
regeneration, which can also alter plant habit.
