Olmos, C. | bioRxiv Science

bioRxiv2024

rpfF is not required for X. translucens pv. undulosa pathogenesis

Bacterial cells self-coordinate via a mechanism called quorum sensing. In Xanthomonas species the gene rpfF encodes the quorum sensing autoinducer synthase. Xanthomonas species are divided into two main phylogenetic groups called Clade I and Clade II. The rpf quorum sensing system has been well studied in multiple Clade II Xanthomonas species and deletion of rpfF resulted in a major loss of virulence on susceptible hosts. However, the only Clade I Xanthomonas species in which the rpfF system was previously studied was in the sugarcane pathogen X. albilineans. In X. albilineans the rpf cluster plays a relatively small role in pathogenesis. Xanthomonas translucens pv. undulosa (Xtu) is a Clade I Xanthomonas species that causes bacterial leaf streak (BLS) and black chaff of wheat and barley and has increased as a concern in recent decades. Neither major resistance nor chemical treatments are available to prevent disease caused by Xtu. Interference with rpf bacterial quorum sensing systems has demonstrated some success in other systems. It was unknown whether BLS caused by Xtu could be prevented via quorum sensing interference. We found that Xtu encodes an rpfF homolog and we created an rpfF knockout mutant to study the role of the rpf system in Xtu. We found that the rpfF mutant was unaffected in its pathogenesis as it caused BLS symptoms and multiplied within wheat plants to the same levels as the wildtype strain. The Xtu rpfF mutant grew normally in lag and log phases in vitro, however it exhibited a shorter stationary phase and an early death phase in plant-derived media. The importance of RpfF in Xtus life cycle is unknown, though it appears to carry out a role in population stability. Our research determined that rpfF is not a major Xtu pathogenicity factor. Therefore, we do not recommend the targeting of the rpf quorum sensing system as a preventative treatment for BLS of wheat.

molecular biology↗

bioRxiv2023

Ketogenic diet administration later in life improves memory and regulates the synaptic cortical proteome through the cAMP/PKA signaling pathway in aging mice.

Aging is a complex biological process that compromises brain function and neuronal network activity, leading to cognitive decline and synaptic dysregulation. In recent years, a cyclic Ketogenic Diet (KD) has emerged as a potential treatment to ameliorate cognitive decline by improving memory in aged mice after long-term administration. However, the molecular mechanisms that govern such changes remains unclear. Additionally, whether short-term cyclic KD administration later in life preserves memory has not been addressed in detail. Accordingly, here we investigated how a short-term cyclic KD starting at 20-23 months-old regulates brain function of aged mice. Behavioral testing and long-term potentiation (LTP) recordings revealed that a cyclic KD improves working memory and hippocampal LTP in 24-27 months-old mice after 16 weeks of treatment. Moreover, the diet also promotes higher dendritic arborization complexity and dendritic spine density in the prefrontal cortex. Furthermore, to elucidate the molecular mechanisms underlying the memory improvements elicited by a cyclic KD, cortical synaptosomes of aged mice fed with this diet for 1 year were analyzed by mass spectrometry. Bioinformatics analysis revealed that long-term cyclic KD administration predominantly modulates the presynaptic compartment by inducing changes in the cAMP/PKA signaling pathway, the synaptic vesicle cycle, and the actin/microtubule cytoskeleton. To test these findings in vivo, synaptic proteins from cortices of 24-27-month-old mice fed with control or cyclic KD for 16 weeks were analyzed by western blot. Interestingly, increased Brain Derived Neurotrophic Factor abundance, MAP2 phosphorylation and PKA activity were observed. Overall, we show that a cyclic KD regulates brain function and memory even when it is administered at late mid-life and significantly triggers several molecular features of long-term administration, including the PKA signaling pathway and cytoskeleton dynamics, thus promoting synaptic plasticity at advanced age.

neuroscience↗