Lack of photosynthetic ability due to altered carbon metabolism is an example of:
Biochemical variation reflects lesions in primary and secondary metabolic pathways rather than chromosome morphology. In heterotrophic tissue culture, selection pressure for photolithotrophy is relaxed, allowing chlorophyll deficient sectors, carotenoid-less callus, or mutants defective in Calvin cycle enzymes Rubisco, phosphoribulokinase, and glyceraldehyde-3-phosphate dehydrogenase to proliferate. Altered carbon metabolism impairs sucrose independence, starch synthesis, or nitrogen assimilation via nitrate reductase and glutamine synthetase deficiency. Such lines require exogenous vitamins, amino acids, or organic acids for survival and turn chlorotic upon transfer to photoautotrophic conditions. Detection uses pigmentation scoring, gas exchange measurement, and enzyme assays. Because defect maps to enzymatic machinery producing sugars and precursors, rather than hormone response or karyotype, it exemplifies biochemical cause of somaclonal variation, often non-revertible without genetic complementation and important when screening for photosynthetic competence of regenerants. Enzymatic assays for Rubisco and chlorophyll fluorescence quantification confirm biochemical deficiency. Unlike reversible habituation, these variants often need genetic complementation or medium supplementation, illustrating how relaxed photoautotrophic selection in tissue culture unmasks metabolic lesions that compromise carbon fixation efficiency in regenerants.
Ref: Taiz & Zeiger Plant Physiology 6th ed Ch 7 photosynthesis; NCBI NBK215354 carbon metabolism; Campbell Biology 12th Ch 10 auxotrophs; Bhojwani Plant Tissue Culture biochemical variation.