Response to strigolactone treatment in chrysanthemum axillary buds is influenced by auxin transport inhibition and sucrose availability

Axillary bud outgrowth is regulated by both
environmental cues and internal plant hormone signaling.
Central to this regulation is the balance between auxins,
cytokinins, and strigolactones. Auxins are transported
basipetally and inhibit the axillary bud outgrowth indirectly
by either restricting auxin export from the axillary buds to
the stem (canalization model) or inducing strigolactone
biosynthesis and limiting cytokinin levels (second messenger
model). Both models have supporting evidence and
are not mutually exclusive. In this study, we used a modified
split-plate bioassay to apply different plant growth
regulators to isolated stem segments of chrysanthemum
and measure their effect on axillary bud growth. Results
showed axillary bud outgrowth in the bioassay within
5 days after nodal stem excision. Treatments with apical
auxin (IAA) inhibited bud outgrowth which was counteracted
by treatments with basal cytokinins (TDZ, zeatin,
2-ip). Treatments with basal strigolactone (GR24) could
inhibit axillary bud growth without an apical auxin treatment.
GR24 inhibition of axillary buds could be counteracted
with auxin transport inhibitors (TIBA and NPA).Treatments with sucrose in the medium resulted in stronger
axillary bud growth, which could be inhibited with apical
auxin treatment but not with basal strigolactone treatment.
These observations provide support for both the canalization
model and the second messenger model with, on the
one hand, the influence of auxin transport on strigolactone
inhibition of axillary buds and, on the other hand, the
inhibition of axillary bud growth by strigolactone without
an apical auxin source. The inability of GR24 to inhibit bud
growth in a sucrose treatment raises an interesting question
about the role of strigolactone and sucrose in axillary bud
outgrowth and calls for further investigation.