The delayed senescence of postharvest buds in salt ions was related to antioxidant activity, HDA9 and CCX1 in broccoli (Brassica oleracea L. var. Italic Planch.)

Abstract

Epigenetic regulation and salt ions play essential roles in senescence control, but the underlying regulatory mechanism of senescence has not been thoroughly revealed in broccoli postharvest buds. Here, we found 200 mmol·L^-1 NaCl, 400 mmol·L^-1 KCl, 40 mmol·L^-1 CaCl₂ and 0.5 μmol·L^-1 Trichostatin-A (TSA, a histone deacetylase inhibitor) delayed the bud senescence. They resulted in significantly inhibiting the malondialdehyde (MDA) content, and dramatically promoting the contents of superoxide dismutase (SOD), peroxidase (POD) and Chlorophyll. Furthermore, the expression of PHEOPHYTINASE (PPH) and NONYELLOWING (NYE1), but not SUPPRESSOR OF OVEREXPRESSION OF CONSTANS 1 (SOC1), were remarkably repressed by salt ions and TSA. Interestingly, HISTONE DEACETYLASE 9 (HDA9) and CATION/Ca²⁺ EXCHANGER 1 (CCX1) were down-regulated by NaCl, CaCl₂ and TSA. Further assays demonstrated that HDA9 could not interact with CCX1 promoter. It suggested that CCX1 along with HDA9 were involved in inhibiting the senescence of broccoli buds, and regulated aging by indirect interaction.

Keywords: Broccoli; CCX1; Chlorophyll (PubChem CID16667503); Dimethy sulfoxide (PubChem CID679); HDA9; Malondialdehyde (PubChem CID10964); Salt ions; Senescence; Trichostatin-A (PubChem CID444732).