Genetic variation in clonal crops arises due to:
In clonally propagated crops meiosis is bypassed, so new genetic variation cannot arise through recombination or independent assortment each generation as in seed crops. Primary sources are somatic mutations in meristematic cells, known as bud sports, and chromosomal aberrations such as polyploidization, aneuploidy, and translocations occurring during mitosis. Transposable element activation, epigenetic changes like methylation shifts, and chimeral segregation also generate variation in long-lived clones. Mutations accumulate over vegetative cycles because they are not filtered by gametophytic selection that normally eliminates deleterious alleles. In potato, somatic mutants for skin color; in apple, bud mutants for maturity; in sugarcane, somaclonal variation from callus culture provide useful variants exploited commercially. Virus-induced variation is pathological, not heritable useful variation. Breeders exploit this rare somatic variability by screening large clonal populations for desirable sports, then isolating and purifying mutant sectors through successive vegetative propagation and meristem culture to stabilize new clone. Epigenetic silencing via small interfering RNAs and methylation changes can create stable phenotypic variants in clones without DNA sequence change, sometimes reversible, adding layer of variation exploitable for selection but also causing unstable off-types that must be rogued during seed certification.
Ref: Dodds JH. Somaclonal variation in clonal crops; Larkin & Scowcroft 1981 Theor Appl Genet