Many flowering plants are hermaphrodite, which poses the problem of self-fertilisation and the subsequent loss of genetic fitness in the offspring. To prevent this, plants have developed a genetically controlled mechanism called self-incompatibility (SI) which allows self (incompatible) pollen to be recognised and rejected before fertilisation can occur. The SI response of Papaver rhoeas (field poppy) has been extensively studied at the molecular and cellular level. Rejection of incompatible pollen occurs on the stigma surface when the pollen S-determinant PrpS, a transmembrane protein, interacts with the stigmatic S-determinant, secreted S-proteins. This triggers a calcium-mediated signalling cascade that targets the cytoskeleton and results in programmed cell death (PCD) of incompatible pollen. Work presented in this thesis investigated the localisation of PrpS and S-proteins. Other studies investigated the role of the cytoskeleton in SI. These demonstrated the involvement of the microtubule cytoskeleton for the first time. Microtubules were rapidly depolymerised and this was implicated in signalling to PCD. The actin cytoskeleton has previously been shown to exhibit biphasic alterations during SI involving depolymerisation, followed by formation of F-actin foci. Studies described here represent the first steps toward characterisation of the F-actin foci. Their potential involvement in PCD and signalling is discussed
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