. As shown in Extended Data Fig. 1a, an ECS signal is visible in P.tricornutum, the characteristics of which depend on the physiological conditions. Deconvolution of the ECS decay-associated spectra (DAS) (see Supplementary Information and Extended Data Fig. 1b,c) explains these observations by revealing the existence of two ECS components (Fig. 1a), respectively characterized by linear and quadratic responses to the ΔΨ (Fig. 1b). The existence of a quadratic ECS, predicted by theory 7 but observed to date only in green algae mutants (Fig. 1c), but was also suppressed by anaerobiosis or by pharmacological inhibition of mitochondrial activity (Fig. 1d, e). This suggests that the PMF is generated in the dark by the plastidial ATPase, which hydrolyses ATP of mitochondrial origin, as previously suggested in green algae 9 .In Viridiplantae (including green algae and higher plants), the AEPs generating additional ATP in the light comprise cyclic electron flow (CEF) around PS1 10 and the water-to-water cycles (WWC). uptake (U 0 ) increased with light, being ~2.5-fold higher at saturating light intensities than in the dark (Extended Data Fig. 2b, d). We further found that the light-stimulated consumption of oxygen was blocked by DCMU (Extended Data Fig. 2c, d), indicating that it was fed by electrons derived from PS2.Moreover, U 0 linearly increased with O 2 evolution, in agreement with earlier findings in the diatom Thalassiosira pseudonana 15, with a slope indicating that ~10% of the electron flow from PSII participate in WWC, regardless of light intensity (Fig 2b). These results indicate that WWC produces a constant extra ATP per photosynthetically-generated NADPH. This is expected for an AEP that contributes to optimizing CO 2 assimilation at any light intensity, and is not the case for CEF, which is completely insensitive to changes in the photosynthetic flux (LEF, Fig 2a).If this WWC is due to the export of photosynthetic products towards the mitochondrial oxidases, then any mitochondrial dysfunction should negatively affect photosynthetic electron transfer rates (ETR PSII ) and light-dependent growth. Mitochondrial respiration comprises a cyanidesensitive pathway (involving Complex III) and an insensitive pathway involving the alternative oxidase (AOX). We therefore modulated mitochondrial activity by adding increasing amounts of Antimycin A (AA) or myxothiazol (Mx), inhibitors of Complex III, in conditions where the AOX was inhibited by SHAM (see legend to Fig. 2d). Both the ΔΨ d and ETR PSII followed respiration linearly (Fig. 2c, d and Extended Data Fig. 3). The almost complete shut-down of respiration resulted in a decrease of photosynthesis which was independent of light intensity (Fig. 3b).Overall we found that in the dark a PMF is generated in the plastid by hydrolysis of ATP produced in mitochondria (Fig 1d,e and Fig. 2c). Conversely, in the light, respiration increases linearly with photosynthesis (Fig. 2b), and vice versa (Fig. 2d). This tight energetic coupling is likely instrumental for adjusting ...

Anatomic abnormalities of the pharynx are thought to play a role in the pathogenesis of obstructive sleep apnea (OSA), but their contribution has never been conclusively proven. The present study tested this anatomic hypothesis by comparing the mechanics of the paralyzed pharynx in OSA patients and in normal subjects. According to evaluation of sleep-disordered breathing (SDB) by nocturnal oximetry, subjects were divided into three groups: normal group (n = 17), SDB-1 (n = 18), and SDB-2 (n = 22). The static pressure-area relationship of the passive pharynx was quantified under general anesthesia with complete paralysis. Age and body mass index were matched among the three groups. The site of the primary closure was the velopharynx in 49 subjects and the oropharynx in only 8 subjects. Distribution of the location of the primary closure did not differ among the groups. Closing pressure (PC) of the velopharynx for SDB-1 and SDB-2 groups (0.90 +/- 1.34 and 2.78 +/- 2.78 cmH2O, respectively) was significantly higher than that for the normal group (-3.77 +/- 3.44 cmH2O; P < 0.01). Maximal velopharyngeal area for the normal group (2.10 +/- 0.85 cm2) was significantly greater than for SDB-1 and SDB-2 groups (1.15 +/- 0.46 and 1.06 +/- 0.75 cm2, respectively). The shape of the pressure-area curve for the velopharynx differed between normal subjects and patients with SDB, being steeper in slope near Pc in patients with SDB. Multivariate analysis of mechanical parameters and oxygen desaturation index (ODI) revealed that velopharyngeal Pc was the only variable highly correlated with ODI. Velopharyngeal Pc was associated with oropharyngeal Pc, suggesting mechanical interdependence of these segments. We conclude that the passive pharynx is more narrow and collapsible in sleep-apneic patients than in matched controls and that velopharyngeal Pc is the principal correlate of the frequency of nocturnal desaturations.

Obesity and craniofacial abnormalities may contribute to the pathogenesis of obstructive sleep apnea. The purpose of this study was to evaluate the influence of body habitus and craniofacial characteristics on types of pharyngeal closure. The types of pharyngeal closure were determined by endoscopic evaluations of closing pressures of the passive pharynx in 54 paralyzed and anesthetized patients with sleep-disordered breathing (SDB). Assessment of craniofacial characteristics of the SDB patients and 24 normal subjects were made by lateral cephalometry. As compared with normal subjects, SDB patients demonstrated receded mandibles and long lower faces with downward mandible development. SDB patients with positive closing pressures at both the velopharynx and oropharynx (VP + OP group) demonstrated smaller maxillas and mandibles than those with positive closing pressures at the velopharynx only (VP-only group). Obesity was more prominent in the VP-only group than in the VP + OP group. Our results suggest that obesity and craniofacial abnormalities contribute synergistically to increases in collapsibility of the passive pharyngeal airway in patients with SDB. Furthermore, the relative contribution of obesity and craniofacial anomaly appears to determine the type of pharyngeal closure in SDB.

Photosynthesis in marine diatoms is a vital fraction of global primary production empowered by CO 2 -concentrating mechanisms. Acquisition of HCO 3− from seawater is a critical primary step of the CO 2 -concentrating mechanism, allowing marine photoautotrophic eukaryotes to overcome CO 2 limitation in alkaline high-salinity water. However, little is known about molecular mechanisms governing this process. Here, we show the importance of a plasma membrane-type HCO 3 − transporter for CO 2 acquisition in a marine diatom. Ten putative solute carrier (SLC) family HCO 3 − transporter genes were found in the genome of the marine pennate diatom Phaeodactylum tricornutum. Homologs also exist in marine centric species, Thalassiosira pseudonana, suggesting a general occurrence of SLC transporters in marine diatoms. Seven genes were found to encode putative mammalian-type SLC4 family transporters in P. tricornutum, and three of seven genes were specifically transcribed under low CO 2 conditions. One of these gene products, PtSLC4-2, was localized at the plasmalemma and significantly stimulated both dissolved inorganic carbon (DIC) uptake and photosynthesis in P. tricornutum. DIC uptake by PtSLC4-2 was efficiently inhibited by an anion-exchanger inhibitor, 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid, in a concentration-dependent manner and highly dependent on Na + ions at concentrations over 100 mM. These results show that DIC influx into marine diatoms is directly driven at the plasmalemma by a specific HCO 3 − transporter with a significant halophilic nature.bicarbonate transporter | chromista | marine environment | sodium-dependent I norganic carbon entry into algal cells is the primary limiting factor for photosynthesis and requires specific transporters (1). The problem is exacerbated especially in marine environment. Specifically, dissolved CO 2 concentrations are low, and the rate of spontaneous CO 2 formation from HCO 3 − is much slower in the ocean relative to freshwater because of the high alkalinity and salinity of seawater (2). Marine diatoms are responsible for one-fifth of global primary productivity and play a key role in global cycles of carbon and other elements (3, 4). The concentration of dissolved CO 2 in seawater under the present atmospheric pCO 2 (below 15 μM at 20°C) is much lower than the K m [CO 2 ] of ribulose-1,5-bisphosphate carboxylase/oxygenase in diatom species (5). Marine diatoms are, thus, believed to rely directly or indirectly on the use of abundant levels of seawater HCO 3 − to support their primary production. The CO 2 -concentrating mechanism (CCM) has been studied extensively in cyanobacteria, and molecular characterizations have revealed a set of CCM components that completely account for the strategy of cyanobacterial tolerance of CO 2 limitation. Freshwater β-cyanobacteria possess three plasma membrane HCO 3