Review: The case for studying mitochondrial function during plant cryopreservation

[Display omitted] •Mitochondria contribute to programmed cell death, redox balance and stress response.•Mitochondrial function is adversely affected in animal cryopreservation.•There is emerging evidence for mitochondrial dysfunction in plant cryopreservation.•Damage can be assessed with new techniques to characterise cell bioenergetics.•Existing mitochondrial interventions may improve cryopreservation survival. Cryopreservation has several advantages over other ex situ conservation methods, and indeed is the only viable storage method for the long term conservation of most plant species. However, despite many advances in this field, it is increasingly clear that some species are ill-equipped to overcome the intense stress imposed by the cryopreservation process, making protocol development incredibly difficult using traditional trial and error methods. Cryobiotechnology approaches have been recently recognised as a strategic way forward, utilising intimate understanding of biological systems to inform development of more effective cryopreservation protocols. Mitochondrial function is a model candidate for a cryobiotechnological approach, as it underpins not only energy provision, but also several other key determinants of germplasm outcome, including stress response, reduction-oxidation status, and programmed cell death. Extensive research in animal cell and tissue cryopreservation has established a clear link between mitochondrial health and cryopreservation survival, but also indicates that mitochondria are routinely subject to damage from multiple aspects of the cryopreservation process. Evidence is already emerging that mitochondrial dysfunction may also occur in plant cryopreservation, and this research can be greatly expanded by using considered applications of innovative technologies. A range of mitochondria-targeted prophylactic and therapeutic interventions already exist with potential to improve cryopreservation outcomes through mitochondrial function.