| Sažetak | Velika većina gljiva su saprofiti, odnosno žive razgrađujući i reciklirajući hranjive tvari od mrtvog biljnog materijala kako bi ponovno postao dostupan biljkama. Postoji širok raspon simbiotskih interakcija biljaka i gljiva, a najčešće uključuju mikorizne i endofitne gljive. Manji broj vrsta gljiva razvio se u smjeru patogenosti sa štetnim učinkom na biljke, a klasificirane su kao biotrofi, nekrotrofi i hemibiotrofi. Biljka je zaštićena staničnom stijenkom koja otežava prodiranje gljive u stanicu pa su rane na biljci ili puči uobičajena mjesta kroz koja patogeni ulaze u biljku. Pojačanja stanične stijenke, poput lignifikacije, suberinizacije, taloženja glikoproteina bogatih hidroksiprolinom i kaloze te umrežavanje proteina stanične stijenke koji ojačavaju mehaničke barijere biljaka i ograničavaju patogene u razvoju, promjene su koje se događaju na mjestima ulaska patogena. Gljive izlučuju enzime koji razgrađuju staničnu stijenku i posjeduju specifične infekcijske strukture, koje se razlikuju ovisno o vrsti gljive. Nadalje, izlučuju efektore kako bi ometale reakcije bazalnih obrambenih mehanizama biljaka, ali biljke su također razvile mehanizme za prepoznavanje takvih molekula. Prepoznavanje efektora u biljkama pokreće obrambene reakcije poznate kao imunitet aktiviran efektorom (eng. effector-triggered immunity, ETI) što rezultira tzv. hipersenzitivnim odgovorom biljke (eng. hypersensitive response, HR) i biosintezom proteina povezanih s patogenezom (eng. pathogenesis-related, PR). Brza proizvodnja ogromnih količina reaktivnih kisikovih vrsta (eng. reactive oxygen species, ROS), takozvani oksidativni prasak, inducira produkciju velikog broja PR proteina. Akumulacija PR proteina na mjestu infekcije obično se povezuje sa sistemski stečenom otpornošću (eng. systemic acquired resistance, SAR), koja se temelji na povećanom stupnju otpornosti distalnih tkiva u slučaju naknadne infekcije patogenim organizmom. |
| Sažetak (engleski) | The vast majority of fungi are saprophytes, which means they live by decomposing and recycling nutrients from dead plant material and make them available for plants to use again. There is a wide range of symbiotic interactions between plants and fungi that most often include mycorrhizae and endophytic fungi. Fewer fungal species have evolved towards pathogenicity with adverse effects on plants and they are classified as biotrophs, necrotrophs, and hemibiotrophs. The plant is protected by a cell wall that makes it difficult for the fungus to penetrate the cell so wounds or stomata are common places through which pathogens enter the plant. Cell wall enhancements such as lignification, suberinization, deposition of hydroxyproline-rich glycoproteins, callose as well as cross-linking of cell wall proteins that strengthen plant mechanical barriers and limit pathogens in development are changes that occur at pathogen entry sites. Fungi secrete cell wall degrading enzymes (CWDE) that break down the cell wall and they possess specific infectious structures which vary widely depending on the type of fungus. Furthermore, they secrete effectors to interfere with the reactions of the basal plant defense mechanisms, but plants have also developed mechanisms to recognize such molecules. The recognition of these effectors in plants triggers defense reactions known as effector-triggered immunity (ETI) which results with a hypersensitive response in host plant (HR) and biosynthesis of pathogenesis-related proteins (PR). The rapid production of large quantities of reactive oxygen species (ROS), the so-called oxidative burst, is inducing the production of a large number of PR proteins. Accumulation of PR proteins at the site of infection is usually associated with the systemic acquired resistance (SAR), which is based on the increased degree of resistance of distal tissues in the event of subsequent infection with a pathogenic organism. |
