Biology subjects

Franklin-Tong, V. E.

Publications and source records attributed to Franklin-Tong, V. E..

3 recordsLinked to original sources

bioRxiv2026

Several plant self-incompatibility systems may be controlled by atypical receptor-ligand interactions

Self-incompatibility (SI) is the single most important mechanism utilized by flowering plants to avoid self-pollination, thus preventing inbreeding and promoting outcrossing. Many plant SI systems are genetically controlled by a multi-allelic S-locus, containing two tightly linked genes that encode the female and male S-determinants. When pollen lands on a "self" pistil, interaction between cognate female and male S-determinants induces an SI signalling response, resulting in the failure of self-fertilization. Here, we review currently known SI systems that utilize receptor-ligand interactions to control pollen rejection on the stigma surface. Although detailed molecular and cellular information is only known for the SI systems in the Brassicaceae and Papaveraceae, it is apparent that the S-determinants of other SI systems (e.g. in the Poaceae and the Convolvulaceae) are likely to also utilize receptor-ligand interactions to prevent self-fertilization. Strikingly, although most of these systems all appear to utilize cysteine rich proteins (CRPs) as ligands to induce an SI response, only one of these receptors is a receptor-like kinase (RLK); the other "receptors" identified to date are proteins of unknown function, which we propose to be atypical receptors (ATRs). Although many of these receptors were identified some time ago, their atypical nature raises many questions, including how they function mechanistically, how they evolved and whether they are found in other plant cell-cell communication systems. Significance StatementSelf-incompatibility involves the precise recognition and rejection of incompatible pollen, often using a receptor-ligand type of interaction between male and female S-determinants. In this review we compare several S-determinants that appear to function as novel, atypical "receptors" (ATRs), with no kinase- or other distinct domains. We propose that the discovery of these novel "receptors" suggests that further, as yet, unidentified ATRs could be more widely utilized in angiosperms than currently appreciated.

plant biology↗

bioRxiv2025

Papaver S-determinants trigger an integrated network of mitochondrially derived ROS and disruption of energy metabolism in incompatible pollen tubes

Many plants use self-incompatibility (SI) mechanisms to prevent inbreeding by inhibiting pollen tube growth in "self" pistils. In Papaver rhoeas, SI is triggered by allele-specific interaction between the pollen and pistil S-determinants, activating a Ca2+-dependent signalling network that leads to rapid reactive oxygen species (ROS) production and eventual programmed cell death (PCD) in incompatible pollen tubes. Expression of the Papaver pollen S-determinant (PrpS) in Arabidopsis thaliana recapitulates Papaver SI when challenged with the cognate pistil ligand (PrsS). Using roGFP2-Orp1, a genetically encoded hydrogen peroxide (H2O2) sensor, combined with measurements of mitochondrial metabolism we have revealed a complex SI response. Within minutes, elevated cytosolic Ca2+ ([Ca2+]cyt) and cytosolic acidification converge to trigger mitochondrial H2O2 production (with consequent cytosolic and plastid H2O2 increase), membrane depolarisation, decreased respiration rate, and ATP depletion. In parallel, oxidative inactivation of cytosolic GAPDH inhibits glycolytic flux, resulting in decreased TCA cycle intermediates and providing a feedback loop to enhance mitochondrial disruption. Preceding production of mitochondrially-sourced ROS, we show that SI rapidly arrests pollen tube growth via inactivation of plasma membrane localised NADPH oxidase (RBOH) mediated superoxide production. Our findings provide new insights into how different ROS signatures from NADPH oxidase and mitochondria drive distinct processes. We demonstrate that mitochondrial disruption is an early and central event in the SI-response, likely driven by positive feedback loops involving altered Ca2+ signalling, cytosolic pH and ROS. Our findings provide novel insights into how SI rapidly disrupts energy metabolism in pollen tubes through interconnected signalling networks centred on mitochondria prior to PCD.

plant biology↗

bioRxiv2021

GPI anchor remodeling by the plant PGAP1 ortholog HLD1 is essential for Papaver self-incompatibility

In eukaryotes, glycosylphosphatidylinositol anchored proteins (GPI-APs) are tethered to the outer leaflet of the plasma membrane where they function as key regulators of a plethora of biological processes. Self-incompatibility (SI) plays a pivotal role regulating fertilization in higher plants through recognition and rejection of self pollen. Here we used Arabidopsis thaliana lines engineered to be self-incompatible by expression of Papaver SI determinants for an SI suppressor screen. We identify HLD1, an ortholog of human GPI-inositol deacylase PGAP1, whose mutation completely abolishes the SI response. We show that HLD1 functions as a GPI-inositol deacylase and that this GPI-remodeling activity is essential for SI. Using GFP-SKU5 as a representative GPI-AP, we show that HLD1 mutation does not affect GPI-AP production and targeting, but alters the configuration of mature GPI-APs. This prevents GPI-AP release from the plasma membrane, suggesting that this process plays a critical role in the regulation of SI. Our data not only identify GPI anchoring as a new pathway of SI providing new directions to investigate SI mechanisms, but identifies for the first time a function for GPI-AP remodeling by inositol deacylation in plants. One sentence summaryThe Papaver self-incompatibility response requires GPI-anchor modification by HLD1, an ortholog of the mammalian PGAP1.

plant biology↗