Ethylene induces cell death at particular phases of the cell cycle in the tobacco TBY-2 cell line

Abstract

It was examined whether ethylene induces programmed cell death in a cell cycle-specific manner. Following synchronization of the tobacco TBY-2 cell line with aphidicolin and its subsequent removal, ethylene was injected into the head space of 300 cm(3) culture flasks at 0 h or 3.5 h later and cells were sampled for 26 h. There were significant increases in cell mortality at G(2)/M in both the 0 h and 3.5 h ethylene treatments, and for the latter treatment, another peak in S-phase. The effect at G(2)/M was greater in the 3.5 h treatment, but was ameliorated by the simultaneous addition of silver nitrate (1.2 microM). In addition, the 3.5 h ethylene treatment resulted in a 1 h delay in the characteristic rise in the mitotic index following aphidicolin-induced synchrony. The addition of silver nitrate alone (1.2 microM), also delayed the entry of cells into mitosis but had no effect on cell cycle length compared with the controls (14 h throughout all treatments) but it induced a peak of mortality 2.5 h after its addition. Nuclear shrinkage was also a characteristic feature of dying cells at G(2)/M. Using Apoptag, an in situ apoptosis detection kit, nuclear DNA fragmentation was observed in the TBY-2 cells which were often isolated on the end of a filament of normal cells. In the 3.5 h ethylene treatment, a marked increase was noted in the percentage of such cells at the G(2)/M transition compared with the controls. Hence, the data show cell death occurring at a major phase transition of the cell cycle and the observations of nuclear shrinkage, isolation of dying cells and nuclear DNA fragmentation suggest a programmed mechanism of cell death exacerbated by ethylene treatment.

Ethylene–auxin interactions regulate lateral root initiation and emergence in Arabidopsis thaliana

“…wei2 and wei7 are less inhibited in lateral root initiation (treated versus untreated: Col 35.5%, wei2 50.9%, wei7 57.1%, P £ 0.02, Student's t-test, n = 14). Ethylene has also been shown to affect the normal cell cycle progression, and to cause DNA endoreduplication in epidermal cells of cucumber hypocotyl (Dan et al, 2003), and to induce cell death at the G2/M boundary in tobacco root cell suspension culture (Herbert et al, 2001). However, ethylene was also recently found to promote division of quiescent center (QC) cells in the Arabidopsis meristem without modifying the QC stem-cell-like properties (Ortega-Martínez et al, 2007).…”

Cell cycle phase‐specific death response of tobacco BY‐2 cell line to cadmium treatment

“…The response of plant cells to various triggers thus probably depends on both their differentiation state and their position in the cell cycle, similar to the situation known from animals. Although the connections between PCD and cell cycle were investigated in plant systems, the studies focused on inducers that were more relevant for differentiated cells (Herbert et al. 2001; Kadota et al.…”

“…Similarly, a rapid decrease in cell viability was induced by pathogen elicitors (Kadota et al. 2004) or certain phytohormones (ethylene –Herbert et al. 2001; jasmonic acid –Swiatek et al.…”

Cadmium‐induced cell death in BY‐2 cell culture starts with vacuolization of cytoplasm and terminates with necrosis

“…The decision on the type of cell‐death response followed is thought to be determined by the nature and intensity of the inducing signal, and the physiological and developmental status of the responding cell or tissue. For example, the morphological features of the PCD response of physiologically homogenous tobacco BY‐2 cells vary substantially depending on the PCD inducer (McCabe and Pennell , Fojtova and Kovarik , Herbert et al , Kadota et al , Kadota and Kuchitsu , Rose et al , Iakimova et al , Reape et al , De Michele et al , Takatsuka et al ) and specifically in case of cadmium treatment, the cell‐death response depends on the concentration of cadmium and on the cell cycle phase. Whereas a high cadmium concentration (1 m M ) caused quick death of the necrotic type, the response to 20 times lower concentration (50 µ M ) was slower and variable within the cell population showing features of both vacuolar and necrotic types (Kuthanova et al ).…”