Migratory species are of special concern in the face of global climate change, since they may be affected by changes in the wintering area, along the migration route and at the breeding grounds. Here we show that migration and breeding times of a trans-Saharan migrant, the pied flycatcher Ficedula hypoleuca, closely follow local temperatures along the migration route and at the breeding grounds. Because of differences in long-term temperature trends of short within-spring periods, the migration period and the time interval between migration and breeding dates of this species have extended in SW Finland. Temperatures in northern parts of Central Europe have risen at the time when the first migrants arrive there, facilitating their migration northward. Temperatures later in the spring have not changed, and the last individuals arrive at the same time as before. The timing of breeding has not advanced because temperatures at the breeding site after arrival have not changed. These results show that the pied flycatchers can speed up their migration in response to rising temperatures along the migration route. Our results strongly indicate that the effects of climate change have to be studied at the appropriate time and geographical scales for each species and population concerned.

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Photosystem II (PSII)-reaction-center protein D1 is encoded by three psbA genes in Synechococcus sp. PCC 7942. The psbAI gene encodes D1 form I (D1 :1) and the psbAII and psbAIII genes encode the transiently expressed D1 form II (D1 :2). We have studied the role of membrane-lipid unsaturation in the expression of psbA genes at low temperature, using a Synechococcus transformant with an increased unsaturation level of membrane lipids. Transfer of the cells from 32°C to 25°C under growth light resulted in the exchange of D1 :1, the prevailing form, for D1 :2 in the wild-type bacterium and the transformant, with no loss of PSII activity. Lowering the temperature further to 18°C caused a drastic decrease in PSII activity in the wild-type bacterium, whereas the transformant was much less affected. Similar decreases in psbAI transcripts and loss of D1 :1 occurred in both strains at 18°C, with concomitant accumulation of psbAII/III transcripts, the latter event being especially prominent in the wild-type bacterium. However, the wild-type bacterium was incapable of accumulating D1:2 to compensate for the loss of D1 :1, which resulted in disassembly of PSII at low temperature. These results imply translational rather than transcriptional regulation of psbA gene expression in Synechococcus 7942 at low temperature, and demonstrate the crucial role of the degree of membrane-lipid unsaturation in promotion of exchange of the D1 protein forms and thus the sustenance of PSII function at low temperature.

In cyanobacterium Synechococcus sp. PCC 7942 the photosystem II reaction-center protein D1 is encoded by three psbA genes. The psbAI gene encodes D1:1 protein, the form used for acclimated growth, and psbAII and psbAIII genes encode the stress-induced form, D1:2 protein. Strong light and low temperature have been shown to induce the expression of psbAII/III genes and down-regulate the expression of psbAI gene. Recently, we reported the involvement of reduced thiols in the up-regulation of psbAII/III genes. In this study, we have analyzed the regulation of psbA gene expression in Synechococcus further, at both the transcriptional and post-transcriptional levels. We show that the inhibitors of the photosynthetic electron-transfer chain, which have different effects on the redox state of the plastoquinone (PQ) pool, have similar effect on the transcription of psbA genes. The inhibitors 3-(3,4 dichlorophenyl)-1,1-dimethylurea (DCMU) and 2,5-dibromo-3-methyl-6-isopropyl-p-benzoquinone (DBMIB) do not cause any changes in psbA gene expression when added under low-light conditions, but dramatically reduce the high-light induction of psbAII/III genes when added upon a high-light shift. Moreover, when the thiol reductant, dithiothreitol, is added to Synechococcus cells together with DCMU concomitant with the high-light shift, no inhibition of psbAII/III gene up-regulation takes place, indicating that the thiol redox state rather than the redox state of the PQ pool regulates psbA gene transcription. We also provide evidence for post-transcriptional regulation of psbA gene expression, particularly, inhibition of translation of psbAI transcripts at high light, and demonstrate that the D1 protein synthesis and degradation processes are coregulated in Synechococcus.

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Three psbA genes encode two different forms of the photosystem II reaction centre protein D1 in Synechococcus sp. PCC 7942. The psbAI gene encoding D1 protein form I (D1:1) is mainly expressed under low growth light conditions while the psbAII and psbAIII genes, encoding D1 protein form II (D1:2), are induced under stress conditions (e.g. high light or low temperature). In this paper we show that psbAII/III genes can be rapidly induced even under low growth light conditions by adding the thiol reductant (DTTred) to Synechococcus cell culture, at a concentration that does not affect cell growth or photosynthetic activity. Similar induction of psbAII/III genes was obtained by illuminating the cells with photosystem I light. In both instances psbAI gene down-regulation coincided with the up-regulation of psbAII/III genes. DTTred-induced exchange in transcript pools was subsequently followed by an exchange of D1:1 for D1:2 at the protein level. Thiol oxidants, iodosobenzoic acid or diamide, reverted the effects of DTTred on psbA gene expression. Thiol oxidants and the thiol-modifying agent N-ethylmaleimide also totally prevented high-light induction of psbAII/III genes. These data strongly suggest that the up-regulation of psbAII/III genes that occurs under stress conditions is mediated by production of thiol reductants, whereas the expression of the psbAI gene is sustained by the more oxidizing conditions that prevail during the steady-state growth of cells.

In cyanobacterium Synechococcus sp. PCC 7942 the photosystem II reaction‐center protein D1 is encoded by three psbA genes. The psbAI gene encodes D1:1 protein, the form used for acclimated growth, and psbAII and psbAIII genes encode the stress‐induced form, D1:2 protein. Strong light and low temperature have been shown to induce the expression of psbAII/III genes and down‐regulate the expression of psbAI gene. Recently, we reported the involvement of reduced thiols in the up‐regulation of psbAII/III genes. In this study, we have analyzed the regulation of psbA gene expression in Synechococcus further, at both the transcriptional and post‐transcriptional levels. We show that the inhibitors of the photosynthetic electron‐transfer chain, which have different effects on the redox state of the plastoquinone (PQ) pool, have similar effect on the transcription of psbA genes. The inhibitors 3‐(3,4 dichlorophenyl)‐1,1‐dimethylurea (DCMU) and 2,5‐dibromo‐3‐methyl‐6‐isopropyl‐p‐benzoquinone (DBMIB) do not cause any changes in psbA gene expression when added under low‐light conditions, but dramatically reduce the high‐light induction of psbAII/III genes when added upon a high‐light shift. Moreover, when the thiol reductant, dithiothreitol, is added to Synechococcus cells together with DCMU concomitant with the high‐light shift, no inhibition of psbAII/III gene up‐regulation takes place, indicating that the thiol redox state rather than the redox state of the PQ pool regulates psbA gene transcription. We also provide evidence for post‐transcriptional regulation of psbA gene expression, particularly, inhibition of translation of psbAI transcripts at high light, and demonstrate that the D1 protein synthesis and degradation processes are coregulated in Synechococcus.

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