Review highlights how somatic mutations and epigenetic changes influence plant adaptability and evolution.
Plant development is characterized by an open growth system, with tissue continuously produced by meristems. Many mature plant cells are not permanently fixed in a state of terminal differentiation. They retain a high degree of developmental plasticity and, under specific conditions (such as injury or hormonal signals), can dedifferentiate, returning to a state similar to that of stem cells, in order to re‐enter the cell cycle, divide and regenerate new organs or entire, fertile plants. Essentially, plants are dynamic systems that continually build, adapt and reprogramme their shape, in contrast to the generally more canalized developmental pathways of animals. In plants, recurrent ontogeny and cellular totipotency allow mutations arising in somatic cells to become heritable if those cells contribute to reproductive tissues, a developmental scenario that is rare or absent in animals. Somatic hereditary changes bridge the gap between somatic variation and germline inheritance, offering unique pathways of adaptation, evolution and reproduction. In this review, we trace how genetic changes become heritable through somatic‐to‐germline transition. Furthermore, we highlight how environmental stressors can induce epigenetic variations, such as alterations in DNA methylation, which can be transmitted to unexposed offspring. Finally, we will discuss how the generation of cellular mosaicism enables us to trace how mutations spread and affect the entire organism, its progeny and its fitness.
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Rogo et al. (2026) studied this question.
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