The transcription of rice plastid psbD-psbC genes encoding photosystem II reaction center protein D2 and chlorophyll alpha-binding protein CP43 is closely regulated by light. To elucidate the sequence requirement for the light-responsive promoter of psbD-psbC operon, transcriptional analysis of the rice promoter was performed with deleted mutants and site-directed mutants in vitro. Deletion of -546 approximately -100 upstream sequences resulted in 4- to 5-fold decrease in the transcription rate. Further deletion of -99 approximately -40 conserved region of repeated sequences resulted in 2-fold decrease in the transcription rate. The core light-responsive promoter requires "-10" element but not "-35" element for accurate initiation of basal transcription. No downstream promoter element was found in the +4 approximately +111 region. The competitive gel-retardation experiments revealed the presence of DNA-binding protein in the rice chloroplasts, which interacts specifically with the -60 approximately -37 repeated sequences. Southwestern blot analysis further demonstrated that the binding factor is composed of 36-kDa polypeptide(s).

Ultraviolet C (UVC) is a DNA damage inducer, and 20 J/m2 of UVC irradiation caused cell growth inhibition and induced cell death after exposure for 24–36 h. The growth of NIH 3T3 cells was significantly suppressed at 24 h after UVC irradiation whereas the proliferation of A431 cells was inhibited until 36 h after UVC irradiation. UVC irradiation increased COX-2 expression and such up-regulation reached a maximum during 3–6 h in NIH 3T3 cells. In contrast, UVC-induced COX-2 reached a maximum after 24–36 h in A431 cells. Measuring prostaglandin E2 (PGE2) level showed a biphasic profile that PGE2 release was rapidly elevated in 1–12 h after UVC irradiation and increased again at 24 h in both cell lines. Treatment with the selective COX-2 inhibitor, SC-791, during maximum expression of COX-2 induction, attenuated the UVC induced-growth inhibition in NIH 3T3 cells. In contrast, SC-791 treatment after UVC irradiation enhanced death of A431 cells. These data showed that the patterns of UVC-induced PGE2 secretion from NIH 3T3 cells and A431 cells were similar despite the differential profile in UVC-induced COX-2 up-regulation. Besides, COX-2 might play different roles in cellular response to UVC irradiation in various cell lines.

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The expression of the plastid photosynthetic psbK‐I‐D‐C gene cluster is closely regulated by light. The time courses of expression of the gene cluster in rice seedlings (Oryza sativa L. cv. Tainong 67) grown under various irradiation regimes were examined by northern and western blot analyses. The data indicated that the gene cluster is photoregulated at the transcriptional and post transcriptional levels. Blue light not only enhanced the accumulation of the overlapping transcripts present in the 7 to 8‐day dark‐grown seedlings, but also induced the accumulation of new class d transcripts encoding D2 protein and CP43. This observation confirms the conservation of blue‐light regulation of psbD‐psbC transcription in plants. In etiolated seedlings, the accumulation of class e transcript encoding CP43 increased most remarkably during development: irradiation further enhanced the transcript level. Although the transcripts encoding D2 protein and CP43 are present in etiolated plants, only D2 protein is accumulated, and CP43 was not detected unless the seedlings were exposed to light. The transcript levels of RNAs d1 and f2 in green seedlings grown under a 12‐h photoperiod exhibited fluctuating patterns over the 24‐h period. The levels o1 RNAs dl and f2 also exhibited significant fluctuation during the 36‐h exposure of the etiolated seedlings to light. These data imply that the circadian regulation of pshD‐psbC expression takes place at the transcriptional and post‐transcriptional levels.