The defensive–offensive associations between algae and herbivores determine marine ecology. Brown algae utilize phlorotannin as their chemical defense against the predator Aplysia kurodai , which uses β-glucosidase ( aku BGL) to digest the laminarin in algae into glucose. Moreover, A. kurodai employs Eisenia hydrolysis-enhancing protein (EHEP) as an offense to protect aku BGL activity from phlorotannin inhibition by precipitating phlorotannin. To underpin the molecular mechanism of this digestive–defensive–offensive system, we determined the structures of the apo and tannic acid (TNA, a phlorotannin analog) bound forms of EHEP, as well as the apo aku BGL. EHEP consisted of three peritrophin-A domains arranged in a triangular shape and bound TNA in the center without significant conformational changes. Structural comparison between EHEP and EHEP–TNA led us to find that EHEP can be resolubilized from phlorotannin precipitation at an alkaline pH, which reflects a requirement in the digestive tract. aku BGL contained two GH1 domains, only one of which conserved the active site. Combining docking analysis, we propose the mechanisms by which phlorotannin inhibits aku BGL by occupying the substrate-binding pocket, and EHEP protects aku BGL against this inhibition by binding with phlorotannin to free the aku BGL pocket.
Photosystem I (PSI) is a multi-subunit pigment-protein complex that functions in light-harvesting and photochemical charge-separation reactions, followed by reduction of NADP to NADPH required for CO 2 fixation in photosynthetic organisms. PSI from different photosynthetic organisms has a variety of chlorophylls (Chls), some of which are at lower-energy levels than its reaction center P700, a special pair of Chls, and are called low-energy Chls. However, the sites of low-energy Chls are still under debate. Here, we solved a 2.04-Å resolution structure of a PSI trimer by cryo-electron microscopy from a primordial cyanobacterium Gloeobacter violaceus PCC 7421, which has no low-energy Chls. The structure shows the absence of some subunits commonly found in other cyanobacteria, confirming the primordial nature of this cyanobacterium. Comparison with the known structures of PSI from other cyanobacteria and eukaryotic organisms reveals that one dimeric and one trimeric Chls are lacking in the Gloeobacter PSI. The dimeric and trimeric Chls are named Low1 and Low2, respectively. Low2 is missing in some cyanobacterial and eukaryotic PSIs, whereas Low1 is absent only in Gloeobacter . These findings provide insights into not only the identity of low-energy Chls in PSI, but also the evolutionary changes of low-energy Chls in oxyphototrophs.
Abstract The defensive-offensive associations between algae and herbivores determine marine ecology. Brown algae utilize phlorotannin as their chemical defense against the predator Aplysia kurodai , which uses β-glucosidase ( aku BGL) to digest the laminarin in algae to glucose. Moreover, A. kurodai employs Eisenia hydrolysis-enhancing protein (EHEP) as an offense to protect aku BGL activity from phlorotannin inhibition by precipitating phlorotannin. To underpin the molecular mechanism of this digestive-defensive-offensive system, we determined the structures of apo and tannic-acid (TNA, a phlorotannin-analog) bound form of EHEP, as well as apo aku BGL. EHEP consisted of three peritrophin-A domains formed in a triangle and bound TNA in the center without significant conformational changes. Structural comparison between EHEP and EHEP–TNA led us to find that EHEP can be resolubilized from phlorotannin-precipitation at an alkaline pH, which reflects a requirement in the digestive tract. aku BGL contained two GH1 domains, only one of which conserved the active site. Combining docking analysis, we propose the mechanisms by which phlorotannin inhibits aku BGL by occupying the substrate-binding pocket, and EHEP protects aku BGL against the inhibition by binding with phlorotannin to free the aku BGL pocket.
We propose a new method to describe three-body breakups of nuclei, in which the Lippmann-Schwinger equation is solved in combination with the complex scaling method. The complex-scaled solutions of the Lippmann-Schwinger equation (CSLS) enable us to treat boundary conditions of many-body open channels correctly and to describe a many-body breakup amplitude from the ground state. The Coulomb breakup cross section from the 6He ground state into 4He+n+n three-body decaying states as a function of the total excitation energy is calculated using CSLS, and the result well reproduces the experimental data. Furthermore, the two-dimensional energy distribution of the E1 transition strength is obtained and the importance of the 5He(3/2−) resonance is confirmed. It is shown that CSLS is a promising method to investigate correlations of subsystems in three-body breakup reactions of weakly bound nuclei.
The defensive-offensive associations between algae and herbivores determine marine ecology. Brown algae utilize phlorotannin as their chemical defense against the predator Aplysia kurodai , which uses β-glucosidase ( aku BGL) to digest the laminarin in algae to glucose. Moreover, A. kurodai employs Eisenia hydrolysis-enhancing protein (EHEP) as an offense to protect aku BGL activity from phlorotannin inhibition by precipitating phlorotannin. To underpin the molecular mechanism of this digestive-defensive-offensive system, we determined the structures of apo and tannic-acid (TNA, a phlorotannin-analog) bound form of EHEP, as well as aku BGL. EHEP consisted of three peritrophin-A domains formed in a triangle and bound TNA in the center without significant conformational changes. Structural comparison between EHEP and EHEP– TNA led us to find that EHEP can be resolubilized from phlorotannin-precipitation at an alkaline pH, which reflects a requirement in the digestive tract. aku BGL contained two GH1 domains, only one of which conserved the active site. Combining docking analysis, we propose the mechanisms by which phlorotannin inhibits aku BGL by occupying the substrate-binding pocket, and EHEP protects aku BGL against the inhibition by binding with phlorotannin to free the aku BGL pocket.
In the experiment using guinea pigs, the accumulated portions of IMP after 125I-IMP microautoradiography were compared in a normal control group and a group exposed to cigarette smoke. In the smoke-exposed lung, the accumulation of silver grains were observed in the alveolar spaces and alveolar macrophages, as well as in the pulmonary capillaries and the alveolar epithelia. After the broncho-alveolar lavage (BAL), increases in alveolar macrophages, total counts of BAL fluid and counts of cell components were seen in the smoke-exposed lung. These results suggested that abnormal function of the pulmonary capillary or alveolar epithelium was wide spread in the smoke-exposed lung.
