TY - JOUR
T1 - Several plant self-incompatibility systems may be controlled by atypical receptor-ligand interactions
AU - Lin, Zongcheng
AU - Bosch, Maurice
AU - Franklin-Tong, Vernonica E.
N1 - Publisher Copyright:
© 2026 The Author(s). The Plant Journal published by Society for Experimental Biology and John Wiley & Sons Ltd.
PY - 2026/4/1
Y1 - 2026/4/1
N2 - Self-incompatibility (SI) is the single most important mechanism utilized by flowering plants to avoid self-fertilization, 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 signaling 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.
AB - Self-incompatibility (SI) is the single most important mechanism utilized by flowering plants to avoid self-fertilization, 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 signaling 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.
KW - Ipomoea
KW - Flowers - physiology - genetics
KW - self‐incompatibility (SI)
KW - Brassica
KW - Poaceae
KW - Signal Transduction
KW - Pollination
KW - S‐determinants
KW - Ligands
KW - atypical receptors (ATRs)
KW - signaling
KW - Papaver
KW - cysteine‐rich proteins (CRPs)
KW - Pollen - physiology - genetics
KW - Self-Incompatibility in Flowering Plants - physiology - genetics
KW - Plant Proteins - metabolism - genetics
KW - Lolium
UR - https://www.scopus.com/pages/publications/105034605139
U2 - 10.64898/2026.02.10.705222
DO - 10.64898/2026.02.10.705222
M3 - Review Article
C2 - 41904645
SN - 0960-7412
VL - 126
JO - Plant Journal
JF - Plant Journal
IS - 1
M1 - e70803
ER -