Plant variegations are characterized by the presence of white sectors in normally green tissues and organs. Whereas the white sectors contain defective plastids that lack coloured pigments, the green sectors contain morphologically normal chloroplasts. Variegation mutants are defective in chloroplast developmental processes and arise due to mutations in nuclear or organellar genes. Despite their widespread occurrence in nature, only a few variegations have been studied at the molecular level. In this review, recent progress toward understanding two Arabidopsis variegations, immutans (im) and var2 is summarized. Both im and var2 are caused by nuclear recessive mutations and the responsible genes have been cloned and characterized. IMMUTANS functions as a chloroplast terminal oxidase that transfers electrons from the plastoquinol pool to oxygen. It appears to be a versatile electron sink, especially early in chloroplast development, when its function is crucial for carotenoid biosynthesis, and in excess light, when it serves as a 'safety valve'. IM also probably functions in chlororespiration. VAR2 encodes a chloroplast FtsH metalloprotease (termed AtFtsH2). Along with other AtFtsH proteins (AtFtsH1, 5 and 8), it forms complexes in the thylakoid membrane that are probably involved in the process of PSII repair during photoinhibition. A model has been proposed to explain the mechanism of var2 variegation, which suggests that threshold levels of FtsH complexes are required for green sector formation. It is concluded that studies on im and var2 have provided novel insights into nuclear-chloroplast interactions and, especially, into mechanisms of photoprotection.