Selective nuclear elimination in multinucleate cells.

نویسندگان

  • Daisuke Maruyama
  • Tomokazu Kawashima
  • Tetsuya Higashiyama
چکیده

A few hours of fumigation will easily eliminate a home's pest infestation. However, one has to choose other means of pest control if the home's residents cannot relocate. The same issue underpins selective nuclear elimination in multinucleate cells. Recently, we reported a novel cell elimination strategy in early developing seeds of the model plant Arabidopsis thaliana; a large embryo-nourishing cell termed the endosperm absorbs the synergid cell [1]. The synergid serves as a beacon for the pollen tube, which conveys the sperm cells, by secreting attractant peptides. After successful fertilization, cell-fusion and subsequent nuclear disorganization rapidly inactivates the synergid, terminating pollen tube attraction and thereby preventing multiple fertilizations of the egg cell. To our surprise, this nuclear elimination is restricted specifically to the synergid-derived nucleus, even though the endosperm-derived nuclei share the same cytoplasm. The endosperm would not produce destructive molecules such as proteases or nucleases because these enzymes would also harm their own nuclei. How then does the endosperm selectively eliminate the synergid-derived nucleus after the synergid-endosperm fusion? In Arabidopsis thaliana, degeneration of the synergid nucleus can be induced by 1-aminocyclopropane-1-carboxylic acid (AAC) treatment even before fertilization. AAC is a precursor of ethylene, a gaseous hormone regulating various developmental processes including fruit ripening and senescence. Ethylene signaling mutants are defective in synergid nuclear degeneration and frequently attract second pollen tubes [2]. However, ethylene signaling is activated not only in the synergid, but also in the zygote and endosperm nuclei soon after fertilization. Furthermore, the cytoplasm of the synergid and endosperm become rapidly mixed through active protoplasmic streaming. Therefore, selective elimination of the synergid nucleus through ethylene signaling should be initiated before the synergid-endosperm fusion although the detailed mechanism is still unclear. After the fusion, the synergid chromosomes appear to segregate, although fail, during the endosperm mitosis. An M-phase marker indicated that the cell cycle of the synergid nucleus is not synchronized with that of the endosperm nuclei, likely causing premature mitotic entry of the synergid nucleus propelled by the actively proliferating endosperm. Another factor controlling the mitosis-associated nuclear elimination is the endosperm-specific Polycomb Repressive Complex 2, FIS-PRC2 [1, 3]. In FIS-PRC2 mutants, the synergid nucleus persists even after several rounds of endosperm proliferation. PRC2 induces gene silencing via tri-methylation of H3K27, suggesting a role for factors downstream of FIS-PRC2. The current model is that 1) after fertilization, the synergid nucleus receives an ethylene signal and becomes susceptible to nuclear …

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عنوان ژورنال:
  • Oncotarget

دوره 6 31  شماره 

صفحات  -

تاریخ انتشار 2015