2025-11-24 ウィスコンシン大学マディソン校(UW–Madison)
<関連情報>
- https://news.wisc.edu/making-lazy-plants-stand-up-research-reveals-new-pathway-plants-use-to-detect-gravity/
- https://www.pnas.org/doi/10.1073/pnas.2510934122
LAZY QUADRUPLE 1の抑制因子はER-細胞膜接触部位で作用し、アラビドプシスの茎における重力屈性経路を制御する SUPPRESSOR OF LAZY QUADRUPLE 1 acts at ER–plasma membrane contact sites to control a gravitropism pathway in the Arabidopsis stem
Takeshi Yoshihara and Edgar P. Spalding
Proceedings of the National Academy of Sciences Published:November 26, 2025
DOI:https://doi.org/10.1073/pnas.2510934122

Significance
Land plants use molecular pathways to convert the gravity vector into a signal that guides the growth of organs. The pathways appear more elaborate with each new finding. Currently we know that LAZY family proteins feature in pathways that guide stem growth upward, roots downward, and branches outward at an intermediate angle. We conducted a genetic screen that identified a protein (SLQ1) in a gravity signaling pathway that operates independently and oppositely of LAZY pathways. SLQ1 functions in endodermal cells at sites where the ER contacts the plasma membrane. The evidence indicates that independent gravity signaling pathways combine in opposition to create a shoot architecture adapted for the conditions, which affects fitness in nature and productivity in crops.
Abstract
LAZY proteins function early in the process of orienting growth of land plants with respect to the gravity vector (gravitropism). In Arabidopsis, an oppositely oriented and LAZY-independent form of gravitropism causes the inflorescence stems of a lazy quadruple mutant (atlazy1;2;3;4) to grow down and along the surface of the soil. Here, we report on a suppressor mutation that restores an upright inflorescence to a plant lacking LAZY functions. The suppressor of lazy quadruple 1 (slq1) mutation alters one amino acid in a protein belonging to the NPH3/RPT2-like (NRL) family. The wild-type SLQ1 protein restores prostrate growth to the atlazy1;2;3;4 mutant when expressed specifically in the gravity-sensing endodermal cells of the stem. The SLQ1 protein interacts head-to-tail with itself and, regardless of direction, with a homologous protein called SETH6. Distinct subcellular bodies apparently containing concentrated head-to-tail SLQ1 oligomers coated with SETH6 occurred primarily at sites of contact between the ER and the plasma membrane (PM), including plasmodesmata. The suppressing slq1 mutation (S149F) prevented these bodies from forming and reinverted the auxin gradient in the atlazy1;2;3;4 inflorescence, switching its gravitropism from downward to upward. Thus, SLQ1 and at least one homolog (SETH6) function at ER–PM contact sites to counter the LAZY-dependent mechanism, not by inhibiting it but by regulating an apparently LAZY-independent gravity-directed process for creating an auxin gradient. Variation in the relative strengths of a LAZY-dependent and a SLQ1-mediated, LAZY-independent process of opposite effect may produce the great variety of stem organ postures observed in nature.


