Unlike unitary animals, vascular plants grow and renew themselves throughout life through meristems — pools of proliferating stem cells — so the relationship between the senescence of individual organs and the ageing of the whole organism is far from trivial. A 2014 New Phytologist commentary by Klimešová, Nobis and Herben tested Howard Thomas's three proposed senescence-avoidance strategies (escape by clonal replacement, resistance by durable organs, pre-emption by programmed death) against comparative flora data for Central European herbs, and added a fourth, previously unconsidered character: adventitious shoot formation, the de novo production of shoots from differentiated cells such as roots. The commentary closed with an unresolved question: it has not been determined whether clonality, organ durability, programmed death, and adventitious shoot formation represent constraints or adaptations with respect to plant ageing; in particular, the role of adventitious shoot formation in preventing the manifestation of senescence due to meristem ageing is unknown; and comparative studies of age-related phenomena across various morphological types are needed.

Background

Ageing and senescence need careful separation in plants. In ecology, senescence means a decline in organismal performance (survival, fecundity, physiology) with age, while ageing is the underlying cumulative process; a plant can therefore show senescence of individual organs while the whole genetic individual persists. Vascular plants are modular: their bodies are built from repeated modules (leaves, shoots, roots) produced by meristems — niches of undifferentiated, proliferating stem cells at shoot and root tips (apical meristems), in leaf axils (axillary meristems), and in cylindrical lateral meristems such as the vascular cambium that thickens stems and roots. Because modules can be replaced, whole-plant senescence is not an automatic consequence of organ senescence.

Several morphological characters govern how a plant's body relates to time. Clonality is vegetative reproduction: new, potentially independent rooting units (ramets) are produced from stolons, rhizomes, or sprouting roots, so that one genetic individual (the genet) can spread and persist for far longer than any of its parts. Organ durability refers to perennial structures, such as the taproot of a perennial herb or the trunk of a tree, that are not replaced if damaged and must last the plant's whole life. Monocarpy is programmed whole-plant death after a single reproductive episode (semelparity), contrasted with polycarpy, repeated reproduction over years. Adventitious shoots are shoots arising not from apical or axillary meristems but from differentiated cells — classically by root sprouting, a capacity present in roughly 8% of the temperate herbaceous flora (Klimešová et al., 2014) — and thus represent meristems created anew rather than inherited from the embryonic axis.

Thomas (2013) organized the field by proposing three strategies by which plants avoid senescence: escaping it through clonal replacement of old modules, resisting it through durable organs, and pre-empting it through programmed death after reproduction, tying these to whether apical meristems remain indeterminate (capable of further vegetative growth) after flowering. Klimešová, Nobis and Herben (2014) tested this framework against large comparative datasets for the Central European herbaceous flora (the CLO-PLA clonal-growth database, growth-ring-based maximum ages for 314 herbs, and phylogenetic analyses of 967 eudicot herbs). They found that indeterminate meristems after flowering occur in only about half of perennial species, so meristem determinacy alone cannot explain monocarpy; that monocarpy has evolved repeatedly and is better viewed as a response to regimes of external mortality; that the inability to replace the primary shoot and main root appears to limit lifespan, with old individuals decaying from their oldest parts; and — counterintuitively — that non-clonal polycarpic herbs reach greater maximum ages than clonal ones. Crucially, they noted that adventitious shoot formation might protect a plant from mutations accumulated in long-lived apical and axillary meristem lineages (a mechanism documented in a long-lived clonal aspen by Ally, Ritland and Otto, 2010, who found somatic mutations accumulating with clonal age) and can supply new meristems when all stem parts are lost — but whether it actually prevents the manifestation of senescence from meristem ageing was unknown. Related observations sharpen the puzzle: old Scots pines show no signs of meristem senescence (Mencuccini et al., 2014), yet the vascular cambium of 600-year-old ginkgo trees retains vitality and disease-defence gene expression without a detectable senescence program (Wang et al., 2020), while whole-tree physiological decline with age is still argued to exist (Munné-Bosch, 2020), and measurable whole-plant senescence has been demonstrated in a perennial herb (Quarles and Roach, 2019).

What remains unresolved is the evolutionary interpretation of this web of associations: for each of the four characters — clonality, organ durability, programmed death, and adventitious shoot formation — does its link to lifespan and age-related decline reflect a non-adaptive morphological constraint (an unavoidable byproduct of how the body is built) or an adaptation (a trait shaped by selection for avoiding senescence)? And, most specifically, does the de novo origin of adventitious meristems from differentiated cells reset or avoid the meristem ageing that would otherwise manifest as whole-plant senescence?

Problem Statement

Determine, by comparative analysis of age-related phenomena across plant morphological types, combined where needed with experiments: (i) for each of the four morphological characters — clonal growth, durability of perennial organs (such as the primary shoot and main root), programmed death after reproduction (monocarpy), and adventitious shoot formation — whether the character acts as a constraint on or an adaptation to whole-plant ageing, i.e. whether its association with lifespan and with age-related decline in survival, physiology or fecundity reflects a non-adaptive structural limit of the plant body or a trait shaped by selection for avoiding or delaying senescence; and (ii) in particular, whether adventitious shoot formation — the de novo origin of meristems from differentiated cells — prevents the manifestation of senescence attributable to meristem ageing, for example by resetting or bypassing the accumulation of somatic mutations, epigenetic changes, or proliferative decline in long-lived apical and axillary meristem lineages. The overarching objective is a coherent account, grounded in genet-level age and fitness data across morphological types, of how plant body architecture and the evolutionary interpretation of its characters jointly determine whether, and why, whole plants senesce or escape senescence. All parts of the question are jointly required: each of the four character determinations in (i) and the mechanistic determination in (ii) must be resolved, with the age and fitness evidence for each stated explicitly, and the overarching account is the integration of these determinations rather than a substitute for any one of them.

References

  1. Klimešová J, Nobis MP, Herben T (2014). Senescence, ageing and death of the whole plant: morphological prerequisites and constraints of plant immortality. New Phytologist 206(1):14–18. doi:10.1111/nph.13160, https://doi.org/10.1111/nph.13160
  2. Thomas H (2013). Senescence, ageing and death of the whole plant. New Phytologist 197(3):696–711. doi:10.1111/nph.12047, https://doi.org/10.1111/nph.12047
  3. Ally D, Ritland K, Otto SP (2010). Aging in a long-lived clonal tree. PLoS Biology 8(8):e1000454. doi:10.1371/journal.pbio.1000454, https://doi.org/10.1371/journal.pbio.1000454
  4. Mencuccini M, Oñate M, Peñuelas J, Rico L, Munné-Bosch S (2014). No signs of meristem senescence in old Scots pine. Journal of Ecology 102(3):555–565. doi:10.1111/1365-2745.12219, https://doi.org/10.1111/1365-2745.12219
  5. Martínková J, Šmilauer P, Mihulka S, Latzel V, Klimešová J (2016). The effect of injury on whole-plant senescence: an experiment with two root-sprouting Barbarea species. Annals of Botany 117(4):667–679. doi:10.1093/aob/mcw010, https://doi.org/10.1093/aob/mcw010
  6. Salguero-Gómez R (2018). Implications of clonality for ageing research. Evolutionary Ecology 32(1):9–28. doi:10.1007/s10682-017-9923-2, https://doi.org/10.1007/s10682-017-9923-2
  7. Heide OM (2019). Juvenility, maturation and rejuvenation in plants: adventitious bud formation as a novel rejuvenation process. The Journal of Horticultural Science and Biotechnology 94(1):2–11. doi:10.1080/14620316.2018.1482795, https://doi.org/10.1080/14620316.2018.1482795
  8. Quarles BM, Roach DA (2019). Ageing in an herbaceous plant: increases in mortality and decreases in physiology and seed mass. Journal of Ecology 107(3):1409–1418. doi:10.1111/1365-2745.13098, https://doi.org/10.1111/1365-2745.13098
  9. Herben T, Klimešová J (2020). Evolution of clonal growth forms in angiosperms. New Phytologist 225(2):999–1010. doi:10.1111/nph.16188, https://doi.org/10.1111/nph.16188
  10. Wang L, Cui J, Jin B, Zhao J, Xu H, Lu Z, Li W, Li X, Li L, Liang E, Rao X, Wang S, Fu C, Cao F, Dixon RA, Lin J (2020). Multifeature analyses of vascular cambial cells reveal longevity mechanisms in old Ginkgo biloba trees. Proceedings of the National Academy of Sciences 117(4):2201–2210. doi:10.1073/pnas.1916548117, https://doi.org/10.1073/pnas.1916548117
  11. Munné-Bosch S (2020). Long-lived trees are not immortal. Trends in Plant Science 25(9):846–849. doi:10.1016/j.tplants.2020.06.006, https://doi.org/10.1016/j.tplants.2020.06.006
  12. Pérez-Llorca M, Munné-Bosch S (2021). Aging, stress, and senescence in plants: what can biological diversity teach us? GeroScience 43(1):167–180. doi:10.1007/s11357-021-00336-y, https://doi.org/10.1007/s11357-021-00336-y
  13. Popov VN, Syromyatnikov MY, Franceschi C, Moskalev AA, Krutovsky KV (2022). Genetic mechanisms of aging in plants: what can we learn from them? Ageing Research Reviews 77:101601. doi:10.1016/j.arr.2022.101601, https://doi.org/10.1016/j.arr.2022.101601
  14. Mašková T, Herben T, Hošková K, Koubek T (2022). Shoot senescence in herbaceous perennials of the temperate zone: identifying drivers of senescence pace and shape. Journal of Ecology 110(6):1296–1311. doi:10.1111/1365-2745.13870, https://doi.org/10.1111/1365-2745.13870
  15. Karami O, Mueller-Roeber B, Rahimi A (2023). The central role of stem cells in determining plant longevity variation. Plant Communications 4(5):100566. doi:10.1016/j.xplc.2023.100566, https://doi.org/10.1016/j.xplc.2023.100566
  16. Fojtová M, Procházková Schrumpfová P, Fajkus J (2025). The leaves fall, yet the tree endures. Cellular and Molecular Life Sciences 82(1):article 368. doi:10.1007/s00018-025-05874-8, https://doi.org/10.1007/s00018-025-05874-8
  17. Santos da Silva G, Harris T, Ferraro A, Millan M, Klimešová J (2026). Throwing away to survive: rhizome senescence as a strategy adopted by an herbaceous clonal plant to remain young forever. Annals of Botany, article mcag004 (advance publication). doi:10.1093/aob/mcag004, https://doi.org/10.1093/aob/mcag004
  18. Klimešová J, Mráz P, Oborny B, Harris T, Santos da Silva G, Ferraro A, Doležal J, Millan M (2026). Determining the age of clonal plants: challenges and prospects. Trends in Ecology & Evolution 41(2):158–169. doi:10.1016/j.tree.2025.10.010, https://doi.org/10.1016/j.tree.2025.10.010