GAMT2 is predominantly expressed in developing seeds and siliques, where it modulates GA levels to ensure proper seed maturation and germination. Overexpression of GAMT2 phenocopies GA-deficient mutants, causing dwarfism, delayed flowering, and reduced fertility . Knockout mutants accumulate active GAs, leading to hypersensitivity to GA biosynthesis inhibitors (e.g., ancymidol) .
While direct data on commercial GAMT2 antibodies is limited, studies on analogous enzymes (e.g., GAMT1) provide insights:
Antigen Source: Recombinant GAMT2 protein purified from heterologous systems (e.g., E. coli or insect cells).
Host Species: Typically rabbit, goat, or mouse for polyclonal/monoclonal antibodies.
Epitope Targeting: Likely regions with conserved functional motifs (e.g., SAM-binding domains).
GA Metabolism: Antibodies enable quantification of GAMT2 protein levels, correlating enzyme activity with GA methylation rates .
Seed Development: Immunolocalization studies reveal GAMT2’s role in regulating GA inactivation during seed maturation .
| Parameter | GAMT2 | GAMT1 |
|---|---|---|
| Primary Substrate | GA4, GA34 | GA9, GA20 |
| Expression Timing | Peak in mature seeds | Peak in early siliques |
| Phenotypic Impact | Dwarfism, reduced fertility | Similar to GAMT2 overexpression |
Antibody Specificity: Cross-reactivity with GAMT1 or other SABATH family members may occur, necessitating rigorous validation .
Signal Sensitivity: Low GAMT2 expression in non-seed tissues may require optimized detection protocols (e.g., signal amplification) .