Neuroligins belong to a highly conserved family of cell adhesion molecules that have been implicated in synapse formation and function. However, the precise in vivo roles of Neuroligins remain unclear. In the present study, we have analyzed the function of Drosophila neuroligin 2 (dnl2) in synaptic development and function. We show that dnl2 is strongly expressed in the embryonic and larval CNS and at the larval neuromuscular junction (NMJ). dnl2 null mutants are viable but display numerous structural defects at the NMJ, including reduced axonal branching and fewer synaptic boutons. dnl2 mutants also show an increase in the number of active zones per bouton but a decrease in the thickness of the subsynaptic reticulum and length of postsynaptic densities. dnl2 mutants also exhibit a decrease in the total glutamate receptor density and a shift in the subunit composition of glutamate receptors in favor of GluRIIA complexes. In addition to the observed defects in synaptic morphology, we also find that dnl2 mutants show increased transmitter release and altered kinetics of stimulus-evoked transmitter release. Importantly, the defects in presynaptic structure, receptor density, and synaptic transmission can be rescued by postsynaptic expression of dnl2. Finally, we show that dnl2 colocalizes and binds to Drosophila neurexin (dnrx) in vivo. However, whereas homozygous mutants for either dnl2 or dnrx are viable, double mutants are lethal and display more severe defects in synaptic morphology. Altogether, our data show that, although dnl2 is not absolutely required for synaptogenesis, it is required postsynaptically for synapse maturation and function.

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With the objective to clarify the physiological significance of polyamines (PAs) in the photosynthetic apparatus, the present study investigated the effects of salt stress with and without foliar application of putrescine (Put) on the structure and function of the photosynthetic apparatus in cucumber. Salt stress at 75 mM NaCl for 7 days resulted in a severe reduction of photosynthesis. The fast chlorophyll afluorescence transient analysis showed that salt stress inhibited the maximum quantum yield of PSII photochemistry (Fv/Fm), mainly due to damage at the receptor side of PSII. In addition, salt stress decreased the density of active reaction centers and the structure performance. The microscopic analysis revealed that salt stress‐induced destruction of the chloroplast envelope and increased the number of plastoglobuli along with aberrations in thylakoid membranes. Besides, salt stress caused a decrease in the content of endogenous PAs, conjugated and bound forms of spermidine and spermine in particular, in thylakoid membranes. However, applications of 8 mM Put alleviated the salt stress‐mediated decrease in net photosynthetic rates (Pn) and actual efficiency of PSII (ΦPSII). Put increased PAs in thylakoid membranes and overcame the damaging effects of salt stress on the structure and function of the photosynthetic apparatus in salt‐stressed plant leaves. Put application to control plants neither increased PAs in thylakoid membranes nor affected photosynthesis. These results indicate that PAs in chloroplasts play crucial roles in protecting the thylakoid membranes against the deleterious influences of salt stress. In addition, the present results point to the probability that the salt‐induced dysfunction of photosynthesis is largely attributable to the loss of PAs in the photosynthetic apparatus.