1. Repair and regeneration Injury program includes: Injury program New organ initiation Primordium activation (dormant buds) Vascular repair Abscission Damage control

2. Primary signals O 2 C 2 H 4 Δ [IAA] Δ [CK] MeJ or SA Response to injury is local &/or systemic

3. Phenylalanine Cinnamic acid Cinnamyl CoA Chalcone Flavonoids Phytoalexins Ferulic acid PAL Chalcone synthase aa + + Oligos C 2 H 4 MeJ SA Suberin Lignin IAA transport Wall crosslinks + + - + + Proteinase inhibitors Chitinase Systemic = upregulation of PAL and chalcone synthase Damage control, ‘immune’ response in whole body

4. Local response might involve vascular repair Cork forms over injury Parenchyma cells de-differentiate  procambium  vascular tissue –Dedifferentiation doesn’t occur until vasculature is broken –IAA and CK activate dedifferentiation

5. Local response may include organ replacement Dormant primordia released –Leaf –Axillary/lateral buds Stem primordia –Root Root external view of primordia

6. Hormones affect apical dominance; injury to SAM or RAM Stem IAA  apical dominance CK made in roots CK  axillary/lateral bud growth What happens if herbivore removes SAM? Root CK  Root Apical dominance What happens if something chomps on root tip? +IAA - CK + + + + ++

7. Applying what we know Cuttings of stems, tubers, corms –Hybrids –Seedless plants Tissue culture –Orchids; transgenic species; nursery species

8. How do we regenerate organs? Injury causes: Parenchyma cells to dedifferentiate  callus Hormone concentrations to change Relative [IAA] : [CK] important Higher [IAA] promotes root program Higher [CK] promotes stem program CallusCK Root program Shoot program IAA + + - -

9. How else do we apply what we know? Injury, moisture and darkness –Layering –Grafting