Maize mosaic virus (MMV) is a plant virus that is transmitted by the corn planthopper, Peregrinus maidis Ashmead (Hemiptera: Delphacidae) in a persistent and propagative manner. MMV is the causal agent for mosaic disease that can cause significant loss in corn yield. Management is focused on controlling insect vector population. The molecular mechanisms of virus transmission by the insect vector are not fully understood. Previously, we identified a receptor for MMV, the P. maidis syntaxin 18 (PmStx18). PmStx18 interacts with the viral glycoprotein and potentially facilitates MMV recognition and entry into the vector, enabling virus proliferation. Stx18 is a key component of the vesicular trafficking machinery and also plays a critical role in neurotransmitter release in insects. In this work, we investigated the expression of PmStx18 in different developmental stages and major parts of the insect vector. Primers were designed to generate templates for synthesis of double-stranded RNA fragments. A 374-bp amplicon was selected and gene-specific sequences were flanked by T7 promoter sequences for in vitro transcription. Results showed a significant difference in the expression of Stx18 in the different developmental stages of P. maidis but not between male and female adults and major body parts. In vitro transcription products indicated optimal reaction conditions and protocol suitability. The findings establish the initial steps for developing RNAi-based approach in controlling MMV transmission by targeting Syntaxin-18 in P. maidis. Further investigations are needed to evaluate the efficacy of this approach.

A balanced chromosomal translocation disrupting DISC1 (Disrupted in Schizophrenia 1) gene has been linked to psychiatric diseases, such as major depression, bipolar disorder and schizophrenia. Since the discovery of this translocation, many studies have focused on understating the role of the truncated isoform of DISC1, hypothesizing that the gain of function of this protein could be behind the neurobiology of mental conditions, but not so many studies have focused in the mechanisms impaired due to its loss of function. For that reason, we perform an analysis on the cellular proteome of primary neurons in which DISC1 was knocked down with the goal of identifying relevant pathways directly affected by DISC1 loss of function. Using an unbiased proteomic approach, we found that the expression of 31 proteins related to neurodevelopment (e.g. CRMP-2, stathmin) and synaptic function (e.g. MUNC-18, NCS-1) is regulated by DISC1 in primary mouse neurons. Hence, this study reinforces the idea that DISC1 is a unifying regulator of both neurodevelopment and synaptic function, thereby providing a link between these two key anatomical and cellular circuitries.

Cytokinesis is accomplished in higher plants by the phragmoplast, creating and conducting the cell plate, to separate daughter nuclei by a new cell wall. The microtubule-severing enzyme p60-katanin plays an important role in the centrifugal expansion and timely disappearance of phragmoplast microtubules. Consequently, aberrant structure and delayed expansion rate of the phragmoplast occur in p60-katanin mutants. Here, the consequences of p60-katanin malfunction in cell plate/daughter wall formation were investigated by transmission electron microscopy (TEM), while deviations in the chemical composition of cell plate/new cell wall were identified by immunolabeling and confocal microscopy, in root cells of the fra2 Arabidopsis thaliana mutant. It was found that, apart from defective phragmoplast microtubule organization, cell plates/new cell walls appeared also faulty in structure, being unevenly thick and perforated by large gaps. In addition, demethylesterified homogalacturonans were prematurely present in fra2 cell plates, while callose content was significantly lower than in the wild-type. Furthermore, KNOLLE syntaxin disappeared from newly formed cell walls in fra2 earlier than in the wild-type. Taken together, these observations indicate that delayed cytokinesis, due to faulty phragmoplast organization and expansion, results in a loss of synchronization between cell plate growth and its chemical maturation.