WormBase Tree Display for Interaction: WBInteraction000501465
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| WBInteraction000501465 | Interaction_type | Regulatory | |||
|---|---|---|---|---|---|
| Interactor | Interactor_overlapping_gene | WBGene00003196 | Interactor_type | Trans_regulated | |
| Expr_pattern | Expr2739 | ||||
| Antibody | WBAntibody00000526 | ||||
| WBGene00002694 | Interactor_type | Trans_regulator | |||
| Variation_interactor | WBVar00000674 | Interactor_type | Trans_regulator | ||
| WBVar00242654 | Interactor_type | Trans_regulator | |||
| Interaction_summary | MEL-11 localization was examined in let-502 mutants using the strong let-502(ca201) allele. MEL-11 remained mostly cytoplasmic with punctate cell membrane localization, similar to its distribution wild-type embryos prior to elongation. Because let-502(ca201) mutant embryos arrest at the onset of elongation, disrupted staining could arise as a secondary consequence of developmental arrest. Therefore, MEL-11 localization was examined again in a partial loss-of-function let-502(sb106) mutant, which does elongate. Although less dramatic compared with the strong allele let-502(ca201), higher levels of cytoplasmic MEL-11 was again found in the let-502(sb106) embryos compared with wild type. This suggests that the disappearance of the cytoplasmic MEL-11 pool, which occurs at the onset of elongation and which could potentially inhibit myosin activity, is at least partly dependent on let-502(+) activity. This is consistent with the antagonistic genetic interactions of let-502 and mel-11. | ||||
| Detection_method | Antibody | ||||
| Regulation_result | Positive_regulate | Life_stage | WBls:0000015 | ||
| Subcellular_localization | membrane | ||||
| Paper | WBPaper00006149 |
