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|Title: ||Molecular and genetic characterization of somaclonal variation in micropropagated banana (Musa spp.)|
|Authors: ||Leela, Sahijram|
Jaya R, Soneji
Madhugiri, Nageshwar Rao
|Issue Date: ||2010|
|Publisher: ||GSB Journals|
|Citation: ||Leela Sahijram, Jaya R. Soneji and Madhugiri Nageshwar Rao. 2010. Molecular and genetic characterization of somaclonal variation in micropropagated banana (Musa spp.). GSB Journals, Vol. 4 (Tree Genetics, Genomics & Genetic Transformation), (in press, page numbers to be assigned) [IIHR Contribution No. 16/2009 vide F.No.RMCU/1.7.6/2009/554 dated 3rd June 2009]|
|Abstract: ||Somaclonal variation (SV) is a phenotypic variation either genetic or epigenetic in origin displayed among somaclones (soma = vegetative, clone = identical copy) and occurs among plants regenerated from tissue culture. SV can be problematic during micropropagation, in vitro conservation and in genetic transformation of crop plants, although, it may be put to good use as a tool in plant breeding. Early detection of SV is, therefore, very useful. In banana, a globally important fruit crop that is extensively micropropagated, it is even more pertinent to study SV as the crop is especially prone to this phenomenon. Shoot-tip culture preserves genetic stability much better than callus or cell suspension cultures, yet somaclonal variation appears to be widespread among plants regenerated from banana shoot-tip cultures. Off-type frequencies vary from 1% to 74%.
To date, somaclonal variation affecting in vitro propagated banana is not well understood, suggesting a complex genetic cause of this phenomenon. A molecular biology-based approach of analysis would help throw light on causes and detection of variants to cure this scourge of the banana micropropagation industry. In vitro conditions can induce mitotic instability. Labile portions are known to exist in the genome rendering it susceptible. These portions get modulated when cells undergo ‘stress’ in tissue culture, resulting in higher re-arrangement and mutation rates than other portions of the genome. Occurrence of hot-spots of mutation and recurring menus of alternative alleles is consistent with this response being limited to a sub-fraction of the genome.
There are identifiable and predictable DNA markers for early diagnosis of SV. DNA methylation has been recognized to cause SV. Representational Difference Analysis (RDA) has been employed to isolate unique fragments (‘difference products’) between visible off-types and ‘normal’ tissue culture (TC) derived plants. Various other molecular techniques are available to detect sequence variation between closely related genomes such as those of source plants and somaclones, viz., RAPD, AFLP (including MSAP – Methylation Sensitive Amplification Polymorphism), microsatellites, etc.
Somaclonal variants have also been shown to have gibberellic acid profiles different from those of normal TC plants. Overdosing with cytokinins, culture frequency / number (or both) have all been shown to cause SV. However, genome is the predominant predisposing factor for occurrence of somaclonal variants.|
|Appears in Collections:||Biotechnology|
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