Salt stress represses hypocotyl elongation possibly through ethylene-mediated modulation of SlUVI4 and SlCCS52Btranscription
We investigated tomato hypocotyl growth under salt stress. NaCl with the concentration of 150 mM in the MS medium significantly inhibited the hypocotyl elongation by 39.3% compared to the control, but did not affect the hypocotyl thickening (Figure 8A-C). Cell cycle analysis revealed that the proportion of 2C and 4C nuclei reduced, and 8C and 16C dramatically increased which led to the increase of EI value from 1.01 to 1.19 (Figure 8D). Salt stress significantly promoted SlUVI4 ,SlCCS52A1 and SlCCS52A2 transcription, and inhibitedSlCCS52B transcription (Figure 8E). To determine the role of ethylene under salt stress condition, we applied 10μM ACC in the growth medium and measured hypocotyl growth, cell cycle progression, and the transcription of SlUVI4 and SlCCS52B . The hypocotyl length was reduced by 38.2% and diameter was increased by 17.0% after 10μM ACC treatment (Figure 9A-C). The proportion of 2C and 4C nuclei decreased but 8C and 16C dramatically increased in ACC treatment, which resulted in a higher EI value (Figure 9D). qRT-PCR analysis revealed that the SlUVI4 transcript abundance increased by 32.3% andSlCCS52B transcript abundance decreased by 36.3% in ACC treatment, whereas SlCCS52A1 and SlCCS52A2 transcription were not altered (Figure 9E). Collectively, these data above suggested that salt stress might trigger ethylene production which disrupted the balance between SlUVI4 and SlCCS52B to reprogram cell cycle progression and eventually lead to the alteration of hypocotyl elongation.