EC Number |
General Information |
Reference |
---|
2.5.1.79 | malfunction |
plants containing the mutation of AtACL5 have defective elongation of their stem internodes because cell expansion is reduced |
-, 739287 |
2.5.1.79 | malfunction |
the increase in height in GhACL5-overexpressing plants cannot be attributed to early germination rates. GhACL5-silenced plants show a severe dwarf phenotype |
-, 739287 |
2.5.1.79 | physiological function |
involvement of ACL5 in morphologically necrotic cell death. Thermospermine synthase (ACL5) and diamine oxidase (DAO) expression is needed for zygotic embryogenesis and vascular development in scots pine |
759258 |
2.5.1.79 | physiological function |
the enzyme is involved in synthesis of thermospermidine, which has a toxic effect on pthogen Verticillium dahliae development in a dose-dependent manner |
-, 739287 |
2.5.1.79 | physiological function |
thermospermine levels are controlled by an auxin-dependent feedback loop mechanism in Populus xylem. Negative feedback regulation, increased POPACAULIS5 expression functions to reduce indole-3-acetic acid levels, which in turn prevents further expression of POPACAULIS5, a regulatory mechanism, mediated through auxin and PttHB8, for maintenance of thermospermine homeostasis in secondary xylem tissues of the stem |
739304 |
2.5.1.79 | physiological function |
thermospermine-deficient mutant acl5 shows severe dwarfism and excessive xylem differentiation. Some auxin analogs remarkably enhance xylem vessel differentiation in the acl5 mutant but not in the wild type. The xylem-inducing effect of auxin analogs is clearly suppressed by thermospermine. Auxin analogs promote protoxylem differentiation in roots and cotyledons in the acl5 mutant. The opposite action between thermospermine and auxin in xylem differentiation may be common in different organs and thermospermine might be required for the suppression of protoxylem differentiation |
723393 |