Sulfur deprivation of algal cultures selectively and partially inactivates photosystem II (PSII)-catalyzed O(2) evolution, induces anaerobiosis and hydrogenase expression, and results in sustained H(2) photoproduction for several days. We show that re-addition of limiting amounts of sulfate (1-10 microM final concentration) to the cultures during the H(2)-production phase temporarily reactivates PSII photochemical and O(2)-evolution activity and re-establishes higher rates of electron transport through the photosynthetic electron transport chain. The reactivation of PSII occurs by de novo D1 protein synthesis, but does not result in the re-establishment of aerobic conditions in the reactor, detectable by dissolved-O(2) sensors. However, concomitant H(2) photoproduction is inhibited, possibly due to excessive intra-cellular levels of photosynthetically-evolved O(2). The partial recovery of electron transport rates correlates with the re-oxidation of the plastoquinone (PQ) pool, as observed by pulse-amplitude modulated (PAM) and fluorescence-induction measurements. These results show that the presence of a more oxidized PQ pool releases some of the down-regulation of electron transport caused by the anaerobic conditions.

We studied the regulation of calpains in explants from rat thyroid glands. Collagenase disaggregation decreased proteinase activity in thyrocytes. It was hypothesized that this effect is mediated by heterotrimeric G proteins, protein kinase C, and tyrosine kinase, but not via Ca(2+) and cAMP-dependent signal pathway.

Предложена модельная система in vitro для изучения репарации двухцепочечных разрывов в ДНК с участием белковых экстрактов из высших растений.'Система основана на исследовании возможности гомологической рекомбинации между двумя линейными фрагментами ДНК плазмиды pUC19. Результатом протекания процесса рекомбинации является восстановление структурной целостности гена IacZ плазмиды pUC19 и как следствие-голубой окраски рекомбинантов, растущих на среде с ИПТГ u Z-gal. Двухцепочечный разрыв в плазмидной ДНК моделировался с помощью рестриктаз EcoRI и BglI. Обсуждаются также возможные варианты репарации в данной системе лигированием субстратов или их негомологической рекомбинацией.