[nazuna 04460] Noni Franklin-Tong 教授 ( 英国・バーミンガム大学) セミナーの御案内
10.3.2 4:28 PMより転載
東京理科大学野田キャンパスにおいて、植物の受精における自己非自己の認識(自家
不和合性)のシグナル伝達機構研究で著名な、Franklin-Tong教授によるセミナーを開
催致します。学生や専門外の方にわかりやすいように、入門的な部分から丁寧に講演
される予定です。興味をお持ちの方の御参加をお待ち致しております。
セミナー1: 2010年3月8日(月) 10:00-11:30 東京理科大学野田キャンパス 計算
科学研究センター4階大会議室
Self-incompatibility signalling networks:conversations that tell “self”
pollen to commit suicide
Higher plants produce seed through pollination, using specific interactions
between pollen and pistil to control of pollination at many levels.
Self-Incompatibility (SI) is an important mechanism to prevent inbreeding
and ensures that genetic diversity is maintained. This system presents a
fascinating example of a cell-cell recognition and rejection system in
plants, controlled by a multi-allelic S locus. “Self” (incompatible)
pollen is discriminated from “non-self” (compatible) pollen, by
interaction of pollen and pistil S locus components, and is subsequently
inhibited. We are studying SI in Papaver rhoeas, which uses a
“receptor-ligand” system to trigger Ca2+-dependent signalling. This
interacts with many cellular components that are harnessed into a complex
network to ensure “self” pollen inhibition and eventually programmed cell
death, which is similar to apoptosis. This provides a very neat way to get
rid of unwanted “self” pollen and prevent self-fertilization. I will
provide an overview of this topic.
セミナー2: 2010年3月9日(火) 10:00-11:30 東京理科大学 野田キャンパス 計
算科学研究センター4階大会議室
Recognition of "self" can be deadly: receptor-ligand interactions and
signalling networks that trigger programmed cell death in pollen
Self-incompatibility (SI) is an important mechanism used by many higher
plant species to prevent inbreeding. It is controlled by a multi-allelic S
locus that allows discrimination between “self” (incompatible) pollen from
“non-self” (compatible) pollen, which is allowed to fertilize the plant by
interaction of pollen and pistil S locus components. In Papaver rhoeas, the
pistil S determinant (recently renamed as PrsS, Papaver rhoeas stigma S) is
a small novel protein that acts as a signalling ligand. It interacts with
its cognate pollen S-determinant (Papaver rhoeas pollen S), PrpS. PrpS is
specifically expressed in pollen, is linked to the pistil S gene, and
displays the high polymorphism expected of an S locus determinant. It
encodes a novel ~20 kDa transmembrane protein with no homology to proteins
in existing databases. PrpS was recently shown to be functionally involved
in SI. Identification of PrpS as the Papaver pollen S-determinant strongly
supports the hypothesis that Papaver SI is triggered by a receptor-ligand
interaction. This was originally based on the finding that when PrsS
interacts with incompatible pollen, it triggers increases in cytosolic free
Ca2+. We have recently begun to use electrophysiology to characterize the
currents activated by SI, and speculate that PrpS may function as a channel
or pore protein.
Ultimately, and probably the major target for SI signals is initiation
of programmed cell death (PCD) involving several caspase-like activities in
incompatible pollen. This provides a very neat way to get rid of unwanted
“self” pollen and prevent self-fertilization. I will talk about the
Ca2+-dependent signalling network, and its targets and how we currently
think it is integrated. The actin cytoskeleton seems to be centrally
involved in integrating or signalling to PCD and I will discuss new data
from our SI system relating to this, suggesting polymerization of actin may
be important; analysis of actin-binding proteins that mediate this stage may
provide clues to the story. I will also present unpublished data on reactive
oxygen species (ROS) and nitric oxide (NO) signalling triggered by the SI
response. Recent work has shown that SI-induced caspase-like proteins, such
as DEVDase, have a very narrow acidic pH optimum, which suggests SI might
trigger dramatic changes in the cytosolic pH. We have investigated whether
acidification of the cytosol may be due to disruption of organelles, and I
will present data showing that the vacuolar compartments of SI-induced
pollen tubes undergo reorganization and disintegrate. This SI-induced
disruption could potentially generate the optimal acidic pH for caspase-like
activities which results in PCD in incompatible pollen tubes.
References
Thomas SG, Franklin-Tong VE. (2004). Self-incompatibility triggers
programmed cell death in Papaver pollen. Nature 2004; 429: 305-309.
Thomas SG, Huang S, Li S, Staiger CJ, Franklin-Tong VE. (2006) Actin
depolymerization is sufficient to induce programmed cell death in
self-incompatible pollen. J Cell Biol 174: 221-229.
Bosch M, Franklin-Tong VE. (2007) Temporal and spatial activation of
caspase-like enzymes induced by self-incompatibility in Papaver pollen. PNAS
USA 104: 18327-18332.
de Graaf BHJ, Rudd JJ, Wheeler MJ, Perry RM, Bell EM, Osman K, et al. (2006)
Self-incompatibility in Papaver targets soluble inorganic pyrophosphatases
in pollen. Nature 444: 490-493.
Wheeler MJ, de Graaf BHJ, Hadjiosif N, Perry RM, Poulter NS, Osman K, et al.
(2009) Identification of the pollen self-incompatibility determinant in
P.rhoeas. Nature 459: 992-995.
Poulter NS, Staiger CJ, Rappoport JZ, Franklin-Tong VE. (2010) Actin-binding
proteins implicated in formation of the punctate actin foci stimulated by
the self-incompatibility response in Papaver. Plant Physiol January 15,
2010: pp.109.152066.
東京理科大学野田キャンパスは、東武野田線運河駅（つくばエクスプレス・流山おお
たかの森駅から7分）下車徒歩5分です。
http://www.tus.ac.jp/info/access/nodcamp.html
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朽津 和幸 (Prof. Dr. Kazuyuki KUCHITSU)
