I have been reading this article recently, which claims that photoinhibition of photosystem II can have measurable impacts of chlorophyll fluorescence. This confused me, however, because photoinhibition (at least as the article describes it) occurs mainly in the PSII reaction center, and I had thought that the majority of chlorophyll fluorescence was caused by excitations that form in the antenna and don't reach the reaction center in time before they decay (after all, there are many more antenna chlorophylls than reaction center chlorophylls). With this in mind, how can it be that photoinhibition of the RC modifies the F0 value of chlorophyll fluorescence data?


1 Answer 1


Not an expert in this field, but a dig through the literature seems to indicate that the chlorophyll fluorescence that is generally referred to for measuring photoinhibition is indeed localized to or associated with the PSII reaction center. In case it is in question, there are estimated to be ~100 chlorophylls directly positioned within the PSII.

I don't know the basis of your supposition about the excitations that never reach the reaction center, so I'm not really sure how to address it. This paper writes that the efficiency of excitation reaching the reaction center is actually quite high in realistic physical simulations. A quantity of interest here is $L_D$, the parameter controlling how far an excitation can travel readily through a photosystem before being lost; I was not able to readily find their estimates for this value though:

Most of the LHCIIs in the mixed membrane are surrounded by PSII-S within a radius of $L_D$, which led to the 82% maximum quantum efficiency of the membrane upon uniform chlorophyll a (ChlA) excitation.

This review links chlorophyll fluorescence to PSII phenomenologically and theoretically but does not directly address the mechanism:

Changes in the yield of chlorophyll fluorescence were first observed as early as 1960 by Kautsky and co‐workers (Kautsky et al., 1960). They found that, upon transferring photosynthetic material from the dark into the light, an increase in the yield of chlorophyll fluorescence occurred over a time period of around 1 s. This rise has subsequently been explained as a consequence of reduction of electron acceptors in the photosynthetic pathway, downstream of PSII, notably plastoquinone and in particular, QA. Once PSII absorbs light and QA has accepted an electron, it is not able to accept another until it has passed the first onto a subsequent electron carrier (QB). During this period, the reaction centre is said to be ‘closed’. At any point in time, the presence of a proportion of closed reaction centres leads to an overall reduction in the efficiency of photochemistry and so to a corresponding increase in the yield of fluorescence.

In one rather blithe review, it is suggested that other sources of fluorescence are close to zero at relevant wavelengths, though they only mention PSI as a source:

At room temperature, we assume the variations in the fluorescence signal arise from PSII only and we ignore emission from PSI largely because the signal does not make a significant contribution below 700nm (Butler, 1978; Pfündel, 1998; Baker, 2008)

Looking into the Pfündel paper, they write in turn:

At room temperature, a small fraction of the absorbed light energy is re-emitted as chlorophyll a fluorescence. It is usually assumed that most of this fluorescence is emanated by PSII, and that the PSI contribution is negligibly small (Krause and Weis 1991; Govindjee 1995)

Without following the citation trail any further, it seems that the general assumption in the field is that excitation "lost" to fluorescence of ChlA without a reaction center accepting the energy is pretty negligible. No one seems to be interested in distinguishing the total PSII fluorescence from the PSII fluorescence actually associated with reaction centers. This probably indicates that the two amounts are pretty close to identical.

For some validation of your intuition, this paper writes:

FV/FM works well for plants with Chl a/b antenna systems in which in vivo fluorescence is dominated by emission from Chl a associated with PSII. In phytoplankton, with their diverse antenna systems and thylakoid configurations, FV/FM must be interpreted with more caution [36], [52]. Taxonomic differences in FV/FM can result from contributions to the minimum fluorescence (F0) from pigments outside PSII (see e.g. [53]). Due to the fluorescence from such pigments, the measured values of FV/FM may depend on the excitation and emission wavelengths (unpublished data).

In other words, you need to be careful to account for fluorescence from non-reaction center-associated pigments but it's quantitatively not a large amount (though I haven't yet found a direct estimate despite a lot of looking!).


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