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Exploiting light to drive redox reactions is currently a hot topic since light is considered as an environmentally friendly source of energy. Consequently, cyanobacteria, which can use light e.g., for generating NADPH, are in the focus of research. Previously, it has been shown that various heterologous redox enzymes could be expressed in these microorganisms. Here we demonstrated the successful inducer-free expression of α-keto-acid dehydrogenases (L-HicDH and D-HicDH) from Lactobacillus confusus DSM 20196 and Lactobacillus paracasei DSM 20008 in Synechocystis sp. PCC 6803 ΔhoxYH mutant using replicative plasmids. While the L-HicDH showed poor activity limited by the amount of expressed enzyme, the D-HicDH was applied both in vivo and in vitro, transforming the selected α-keto acids to the corresponding optically pure (R)-α-hydroxy acids (ee >99%) in up to 53% and 90% conversion, respectively. Europäische Kommission 764920 Fundação para a Ciência e a Tecnologia (FCT) (DE-588b)6030623-3 1087594006 IF/00256/2015 Agency for Science Technology and Research (Singapore) (1087594006) SFRH/BD/117508/2016 Version of record

Photobiocatalysis is an alternative approach in synthesis that received much attention in the recent years. Due to the youth of the topic, only few reactor systems are commercially available. To allow a parallel parameter-screening approach as it is often used in the optimization of biocatalytic processes, a photoreactor was developed that can illuminate up to 24 samples at well-defined reaction conditions. The device's optical features and temperature regulation have been thoroughly characterized and its applicability was demonstrated in four examples, including three photobiocatalytic, and one photocatalytic process: (i) The light dependent decarboxylation using a photodecarboxylase; (ii) the reduction of protochlorophyllide using a protochlorophyllide oxidoreductase; (iii) the photosynthetic oxygen production performed by cyanobacteria (iv) the (-)-riboflavin-catalyzed (E/Z)-isomerization of cinnamic acid derivatives. (VLID)6280987 Accepted version

Neograničen proliferativni kapacitet tumora i imortalnih staničnih linija ovisi o sposobnosti održavanja dužine telomera i obično se bazira na aktivaciji telomeraze, RNA-ovisne DNA polimeraze koja reverznom transkripcijom endogenog RNA kalupa sintetizira telomerna ponavljanja izravno na krajevima kromosoma. Međutim, znatan broj tumora može produživati telomere i bez prisutsva telomeraze mehanizmima alternativnog produžavanja telomera (ALT). Temelj ALT-a su replikacijski procesi ovisni o rekombinaciji kod kojih se kao kalup za sintezu dodatnih telomernih ponavljanja mogu koristiti druge telomere ili izvankromosomska telomerna ponavljanja, međutim molekularni procesi nisu razjašnjeni. Aktivnost ALT prepoznata je samo u nenormalnim stanicama i čini se da je njezino djelovanje usko povezano s poremećajem normalne funkcije telomera koja je primarno zaštita krajeva kromosoma kako ne bi bili zamijenjeni za dvolančane lomove nastale oštećenjem. Sukladno tome, samo produžavanje telomera posljedica je stalnog djelovanja stanične mašinerije za popravak na telomernu DNA. Mehanizmi održavanja telomera dobra su meta za razvoj antitumorskih tretmana: pojavljuju se u svim tumorima, većina zdravih stanica ih ne koristi i očekivane su nuspojave takvih tretmana minimalne. Većina istraživanja u tom smjeru provodi se na telomeraznim inhibitorima, međutim, da bi takvi tretmani zaista bili uspješni neophodno je da se u obzir uzme i ALT te da se bolje istraže mehanizmi i genetska podloga njegova djelovanja. Unlimited proliferative capacity of tumor cells and immortal cell lines depends on their ability to maintain their telomeres, usually by activating telomerase, an RNA-dependent DNA polymerase that adds telomere repeats directly on the ends of chromosomes by reverse-transcribing an endogenous RNA template. On the other side, a number of tumors can also lengthen their telomeres without telomerase by means of alternative lengthening of telomeres (ALT). ALT is based on recombination-dependent replication processes that can use other telomeres or extrachromosomal telomeric repeats as templates for telomere elongation. Molecular basis of these processes are not yet clear. ALT activity has only been detected in abnormal cells and it seems that it is closely related to dysfunction in telomeres. These telomere dysfunctions compromise the roles they normally play in chromosome end protection and chromosomal ends are recognized as double stranded breaks caused by DNA damage. The telomere elongation itself is, by that definition, a consequence of cell repair machinery constantly acting on telomeric DNA. Telomere maintenance mechanisms could be used as a good target for cancer treatment because they appear in all tumors but not in healthy cells, so their inhibition should show minimal side-effects. Most research in that direction is based on telomerase inhibitors but for most successful results ALT also needs to be taken in consideration and its mechanisms and genetic background further investigated.