Nitric oxide as a signaling factor to upregulate the death-specific protein in a marine diatom, Skeletonema costatum, during blockage of electron flow in photosynthesis.

To determine the physiological functions of a novel death-specific protein gene, Skeletonema costatum DSP-1 (ScDSP-1) in a marine diatom, Skeletonema costatum, the mRNA abundance of ScDSP-1 was measured in cultures subjected to light manipulation and treatments with various chemicals. When cells were transferred to a dim light intensity of 15 micromol m(-2) s(-1), ScDSP-1 mRNA levels showed a transient increase of 1 to 17.2 micromol (mol 18S rRNA)(-1) in 60 h. Furthermore, treatments with the photoinhibitors 3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU) and 2,5-dibromo-3-methyl-6-isopropyl-p-benzoquinone (DBMIB) resulted in high ScDSP-1 mRNA levels, which reached 943 and 72 micromol (mol 18S rRNA)(-1), respectively. Treatment with the nitric oxide (NO) donor diethylamine nitric oxide also induced ScDSP-1 expression, and this inducible expression was inhibited by the NO scavenger hemoglobin. Additionally, the expression of ScDSP-1 mRNA elicited by DCMU and DBMIB was efficiently reduced when cultures were pretreated with the cell-penetrating NO scavenger 2-(4-carboxyphenyl)-4,5-dihydro-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide. In contrast, treatment with another photoinhibitor, paraquat, had no effect on ScDSP-1 expression. Our results indicated that NO is the crucial secondary messenger which signals the expression of ScDSP-1 when electron flow between photosystem II and photosystem I is blocked in S. costatum cells. In addition, the discovery of a similar gene, ScDSP-2, is briefly described.