HIRD11 promotes plant growth, particularly influencing primary root elongation. Mutants lacking functional HIRD11 exhibit stunted growth, with primary roots 30–40% shorter than wild-type plants . Complementation experiments restoring HIRD11 expression rescue this phenotype, confirming its critical role in development .
| Plant Line | Primary Root Length (mm) | mRNA Abundance (Relative to WT) |
|---|---|---|
| Wildtype (Col-0) | 45.2 ± 2.1 | 1.00 ± 0.05 |
| hird11-1 | 28.7 ± 1.8 | 0.15 ± 0.02 |
| hird11-1 + wtRG4 | 44.5 ± 1.9 | 1.10 ± 0.07 |
| hird11-1 + mutRG4 | 52.3 ± 2.3 | 1.05 ± 0.06 |
HIRD11’s translation is modulated by an RG4 structure in its 3’ untranslated region (UTR) :
RG4 Function: This guanine-rich sequence forms a stable secondary structure in vivo, suppressing translation under normal conditions .
Mutation Impact: Disrupting the RG4 (mutRG4) increases polysome-associated HIRD11 mRNA by 60%, enhancing protein synthesis and unexpectedly elongating roots beyond wildtype levels .
| Parameter | wtRG4 Plants | mutRG4 Plants |
|---|---|---|
| Polysome-associated mRNA (%) | 22 ± 3 | 35 ± 4 |
| Primary Root Length (mm) | 44.5 ± 1.9 | 52.3 ± 2.3 |
Despite HIRD11’s functional importance, no antibody has been commercialized due to:
Technical Limitations: High sequence similarity among dehydrins complicates epitope specificity .
Alternative Methods: Studies rely on polysome profiling and qRT-PCR to quantify translational efficiency .