Global food security is threatened by impending climate change, limited agricultural land
and resources, and by an increase in human population disproportional to the increase in
food production. One way to increase food production is to decrease crop yields lost to
pathogens. Blumeria graminis is an obligate biotrophic fungal pathogen that causes powdery
mildew in wheat and barley. It is an economically important phytopathogen that employs
over 500 effectors to facilitate infection by subduing the plant immune system. In particular,
RNase-like effector proteins associated with haustoria (RALPHs), such as BEC1054/CSEP0064,
are thought to play a crucial role in Blumeria infection. I hypothesised that BEC1054 facilitates
infection by inhibiting host cell death via host ribosome binding. This study focuses
on the relationship between RALPH effector BEC1054 and the barley Jasmonate-induced
protein 60 (JIP60), whose N-terminal domain acts as a ribosome-inactivating protein (RIP).
JIP60 probably induces host cell death by depurination of the SRL site on the 28S rRNA
subunit, leading to ribosome inactivation and translation inhibition. In plants exposed to
methyl-jasmonate, a phytohormone that induces expression of JIPs and results in senescence,
host rRNA degradation was inhibited in transgenic wheat expressing BEC1054. Transient
expression of active recombinant JIP60, via agroin ltration, mediates host cell death in nonnative Nicotiana benthamiana. Conversely, co-expression of BEC1054 with JIP60 in N. ben-
thamiana inhibits the JIP60 RIP-mediated necrosis. So far, no speci c residues have been
identi ed that are involved in BEC1054 function. Therefore, I propose BEC1054 effector employs
a mode of action based on non-speci c factors, such as structural compatibility with its
targets and hydrophobic interactions, rather than complementary hydrophilic residues. The
main function of BEC1054 is to bind host ribosomes and occlude the SRL site. This then inhibits host RIPs from performing rRNA cleavage, which would lead to ribosome inactivation, host cell death and prevent establishment of infection.