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Diplomska naloga obravnava vse trenutno poznane obrambne mehanizme bakterij v boju z bakteriofagi. Tema je razdeljena po sklopih, ki sovpadajo s stopnjami v življenjskem ciklu bakteriofaga. Prva stopnja je preprečitev vezave bakteriofaga na membrano bakterijske celice. Ta poteka tako, da celica blokira dostop do svojih receptorjev. Dostop lahko omeji s tvorbo izvencelične matrice, proizvodnjo maskirnih elementov ali kompetitivnih inhibitorjev. V drugem koraku skuša celica preprečiti vstop tuje DNA v celico po uspešni vezavi bakteriofaga na receptor. Sistemi, ki opravljajo to nalogo, se imenujejo Sie. Neuspešnost Sie sitemov vodi v aktivacijo R-M sistemov, ki razrežejo tujo nukleinsko kislino, preden se ta uspe integrirati v DNA gostiteljske celice. Mehanizem, podoben R-M sistemu, je CRISPR-Cas sistem, ki pa je za razliko od vseh ostalih obrambnih mehanizmov v bakterijski celici edini adaptiven. Ob odpovedi vseh obrambnih mehanizmov se celice zatečejo k samomoru kot altruističnemu načinu obrambe ostalih celic v populaciji. Tega omogočajo Abi in TA sistemi. Interferenca sestavljanja virusov ni bakteriji lasten mehanizem, ampak je pogojen s prisotnostjo parazita. Parazit v obliki avtonomno replikativne DNA zamenja DNA virusa s svojo. Tako prepreči razmnoževanje virusa, a ne prepreči lize celice. Za konec pa opisuje še najnovejši mehanizem obrambe imenovan BREX. The thesis deals with all currently known bacterial defense mechanisms against bacteriophages. The theme is divided into sections that correspond with those of a bacteriophage life cycle. The first step is to prevent the binding of a bacteriophage to the bacterial cell membrane. Cells achieve this by blocking access to their receptor. Access may be limited by the production of an extracellular matrix, masking elements or competitive inhibitors. In the second step, the cell is trying to prevent entry of foreign DNA after a successful phage binding to the receptor. Systems that perform this task are called Sie. Failure of Sie systems leads to the activation of R-M systems, which cut the foreign nucleic acid before it manages to integrate into the DNA of the host cell. Mechanism similar to the R-M system is the CRISPR-Cas system, which, unlike other defensive mechanisms functions as adaptive immunity. If all these systems fail, it leads to the cell resorting to suicide as an altruistic defense for other cells in the population, enabled by Abi and TA systems. Viral assembly interference is not bacteria’s own mechanism, but depends on the presence of a parasite in the form of autonomously replicating DNA. In the process of assembly viral DNA is replaced by the parasite’s. Thereby preventing viral replication, but not preventing host cell lysis. Finally, it describes the latest defense mechanism called BREX.