Light Intensity

Light intensity is another external signal that regulates the development of the photosynthetic apparatus.The photosynthetic bacteria have developed mechanisms to adapt to different light intensities in order to maintain a more constant rate of photosynthetic activity.Cells grow competently in an environment of dim light，and high intensity light represses the formation of the photosynthetic apparatus.Earlier studies indicated that the cellular Bchl content of R.sphaeroides varied in inverse proportion to the incident light intensity（Cohen-Bazire and Kunisawa 1963）.The molar ratio of LH-I to RC Bchl is fixed at about 20 to 25（Agaard and Sistrom 1972）.A shift of R.sphaeroides cells from high light（30 W/m2）to low light（3 W/m2）causes an immediate cessation of cell growth，Bchl accumulation，and protein synthesis.After a short period of adaptation，the cells resume their growth，Bchl synthesis commences at a new and higher rate，and two LH proteins and two additional high-molecular-weight photosynthetic membrane proteins increase threefold to fivefold（Chory and Kaplan 1983）.The increased synthesis of LH antenna proteins as a result of reduction in light intensity results in an increase in the number and size of photosynthetic units per ICM and the number of ICMs per cell（Drews and Oelze 1981；Drews 1986）.Chory and Kaplan（1982）have developed an in vitro transcription-translation system in which the levels of translatable mRNA are correlated with the increased levels of ICM proteins.

The expression of the genes coding for pigment-binding proteins in R.sphaeroides is also inversely correlated to the light intensity（Zhu and Kaplan 1985）.When R.sphaeroides cells were shifted from the light to the dark，the levels of mRNA for LH-Ⅰ，RC-L，and RCM increased in the first five minutes after shifting because of derepression of transcription，although they eventually declined，presumably as a result of shortage of energy generation.Recently we have found that decreased light intensity results in increased levels of mRNAs for LH-Ⅰ，LH-Ⅱ，and RC-L，-M，and-H，as well as Bchl biosynthetic enzymes in R.capsulatus（Zhu and Hearst 1986）.An interesting result is that the crt genes（A，I，B，C，D，E）in R.capsulatus again respond to light intensity in a way opposite to the other photosynthetic genes：increased light intensity leads to increased mRNA levels from these crt genes（Zhu and Hearst 1986）（see Table 1）.Since photo-oxidative killing occurs only in high light and oxygen（Drews and Oelze 1981），and since it is well documented that Crt functions both to harvest light as an auxiliary pigment and to protect the photosynthetic apparatus in all photosynthetic organisms（Cogdell 1978；Halliwell 1984），we proposed that the transcriptional response of crt genes to high light is essential to the function of protecting cells from photo-oxidative damage.It is interesting to note that a very abundant transcript（0.4 kb）from Bam HI-J，whose location does not correspond to the genetically mapped crtF or crtE genes in this fragment as shown by Armstrong and Hearst（unpublished observations），also increases（threefold）in response to high light（Zhu and Hearst 1986）.(https://www.daowen.com)

In contrast to the pigment-binding protein genes，the rbcL gene is positively regulated by light intensity.The increase in light intensity results in an enhancement of both the levels of mRNA and enzymatic activity of RuBPCase in R.sphaeroides（Zhu and Kaplan 1985）.Obviously，the gene for RuBPCase represents another type of regulation in R.sphaeroides.The mechanism by which cells adapt to light intensity is as yet unknown.From the results described here we suggest that the adaptation may take place at the transcriptional level.Another speculation is that variations of light intensity regulate the biosynthesis of the pigment complexes via the redox state of enzymes or regulatory proteins（Drews and Oelze 1981）.Recently a sequence region of at least 300—700 bp 5'of promoter function of the puf operon was found to be essential for light regulation（Kaplan，personal communication）.