Enhanced Age-Related Resistance to Tomato Yellow Leaf Curl Virus in Tomato Is Associated With Higher Basal Resistance

Tomato yellow leaf curl virus (TYLCV) is one of the most notorious plant pathogens affecting the production of tomato worldwide. While the occurrence of age-related resistance (ARR) against TYLCV has been reported, the factors impacting its development remain unknown. We conducted a series of experiments with three tomato cultivars that vary in basal resistance to TYLCV to explore factors involved in the development of ARR. Our data indicate that ARR is more pronounced in tomato cultivars with higher basal resistance. Additionally, increased plant biomass in older plants does not contribute to ARR. Virus source plants with a younger age at initial inoculation facilitates virus acquisition by whiteflies. Finally, an analysis on plant hormones suggests that salicylic acid (SA) may play a major role in the development of ARR in tomato against TYLCV. These findings provide new insights into the developmental resistance in tomato against TYLCV as well as clues for the deployment of ARR in the management of diseases caused by TYLCV.

Physical and Chemical Barriers in the Larval Midgut Confer Developmental Resistance to Virus Infection in Drosophila

Insects can become lethally infected by the oral intake of a number of insect-specific viruses. Virus infection commonly occurs in larvae, given their active feeding behaviour; however, older larvae often become resistant to oral viral infections. To investigate mechanisms that contribute to resistance throughout the larval development, we orally challenged Drosophila larvae at different stages of their development with Drosophila C virus (DCV, Dicistroviridae). Here, we showed that DCV-induced mortality is highest when infection initiates early in larval development and decreases the later in development the infection occurs. We then evaluated the peritrophic matrix as an antiviral barrier within the gut using a Crystallin-deficient fly line (Crys−/−), whose PM is weakened and becomes more permeable to DCV-sized particles as the larva ages. This phenotype correlated with increasing mortality the later in development oral challenge occurred. Lastly, we tested in vitro the infectivity of DCV after incubation at pH conditions that may occur in the midgut. DCV virions were stable in a pH range between 3.0 and 10.5, but their infectivity decreased at least 100-fold below (1.0) and above (12.0) this range. We did not observe such acidic conditions in recently hatched larvae. We hypothesise that, in Drosophila larvae, the PM is essential for containing ingested virions separated from the gut epithelium, while highly acidic conditions inactivate the majority of the virions as they transit.

Methylation-directed Acetylation of Histone H3 Regulates Developmental Sensitivity to Histone Deacetylase Inhibition

BackgroundTreatment of cells with hydroxamate-based lysine deacetylase inhibitors (KDACis) such as Trichostatin A (TSA) can induce biological effects such as differentiation or apoptosis of cancer cells, and a number of related compounds have been approved for clinical use. TSA treatment induces rapid initial acetylation of histone 3 (H3) proteins which are already modified by tri-methylation on lysine 4 (H3K4me3) while acetylation of bulk histones, lacking this mark, is delayed. Sgf29, a subunit of the SAGA acetyltransferase complex, interacts with H3K4me3 via a tandem tudor domain (TTD) and has been proposed to target the acetyltransferase activity to H3K4me3. However the importance of acetylation of this pool of H3 in the biological consequences of KDACi treatment is not known.ResultsWe investigated the role of H3K4me3-directed acetylation in the mechanism of action of TSA on inhibiting development of the eukaryotic social amoeba Dictyostelium discoideum. Loss of H3K4me3 in strains with mutations in the gene encoding Set1 or the histone proteins confers resistance to TSA-induced inhibition of development and delays accumulation of histone acetylation on H3K9 and K14. A candidate orthologue of Sgf29 in Dictyostelium has been identified which specifically recognizes the H3K4me3 modification via its tandem Tudor domain (TTD). Disruption of the gene encoding Sgf29 delayed accumulation of H3K9Ac, abolished targeted H3K4me3-directed H3Ac and led to developmental resistance to TSA, which is dependent on a functional TTD. TSA resistance also results from overexpression of Sgf29.ConclusionPreferential acetylation of H3K4me3 histones, regulated by Sgf29 via its TTD, is important in developmental sensitivity to TSA. Levels of H3K4me3 or Sgf29 will provide useful biomarkers for sensitivity to this class of chemotherapeutic drug.

Autographa californica M nucleopolyhedrovirus early GP64 synthesis mitigates developmental resistance in orally infected noctuid hosts

The unusual early synthesis of the Autographa californica M nucleopolyhedrovirus (AcMNPV) budded virus (BV) structural protein GP64 is an important virulence factor during oral infection of Heliothis virescens larvae. Considering the breadth of the AcMNPV host range, the importance of early GP64 synthesis in orally infected permissive hosts (Trichoplusia ni and Spodoptera exigua) from subfamilies other than that of H. virescens was assessed. An AcMNPV recombinant, having wild-type early and late GP64 synthesis, was compared with one in which only late GP64 synthesis occurred. Early GP64 synthesis was found to have more of an effect on virulence in orally inoculated T. ni than S. exigua and that virulence was dependent on two factors: the ability of the host to slough occlusion-derived virus (ODV)-infected midgut cells and the rapidity with which BV was transmitted to the tracheal cells. In both host species, insects inoculated orally with the control virus transmitted BV to tracheal cells hours before those inoculated with the gp64 temporal mutant. Moreover, with early GP64 synthesis, the lag between the onset of viral gene expression in midgut and tracheal cells was only 3–4 h, supporting the conclusion that in these insects, the first systemic infections arose from ODV-derived nucleocapsids repackaged as BV. These results provide further empirical proof that early GP64 synthesis is a component of a unique and selectively advantageous baculovirus infection strategy for exploiting larval lepidopterans by counteracting developmental resistance.