Biology subjects

Padula, L.

Publications and source records attributed to Padula, L..

3 recordsLinked to original sources

bioRxiv2025

Auxin antagonism of ABA-induced stomatal closure in Arabidopsis requires the TIR1/AFB-AUX/IAA module and ROS suppression

Auxin inhibits ABA-induced stomatal closure, yet the underlying mechanism remains unclear. In this work we quantified 3-Indoleacetic acid (IAA) inhibition of ABA-triggered closure in Arabidopsis thaliana mutants and transgenic plants and observed that IAA inhibition of ABA-induced stomatal closure was lost or weakened in tir1-1 and axr3-1 mutants, affected in auxin perception. The same was found in aux1-7, yuc5/8/9 and pils5-2/2-5 mutants, and in YUCCA8 and PILS5 overexpressors, all altered in auxin synthesis or transport. Stomatal sensitivity to IAA was also reduced in phyB-9 and rbohd, toc1 and cca1/lhy mutants, in certain ecotypes, and in response to mild drought. H+-ATPase mutant aha2-5 showed reduced stomatal sensitivity to IAA at 22{degrees}C but not at 35{degrees}C, while high-temperature-induced stomatal opening was not affected in tir1-1. IAA also caused partial degradation of the DII-VENUS auxin reporter, and inhibited ABA-induced ROS production in guard cells. Our results show that IAA counteracts ABA signalling via the TIR1/AFB-AUX/IAA module and ROS suppression, with genetic factors and mild drought modulating the response.

plant biology↗

bioRxiv2020

Induction of SARS-CoV-2 protein S-specific CD8+ T cells in the lungs of gp96-Ig-S vaccinated mice

Given the aggressive spread of COVID-19-related deaths, there is an urgent public health need to support the development of vaccine candidates to rapidly improve the available control measures against SARS-CoV-2. To meet this need, we are leveraging our existing vaccine platform to target SARS-CoV-2. Here, we generated cellular heat shock chaperone protein, glycoprotein 96 (gp96), to deliver SARS-CoV-2 protein S (spike) to the immune system and to induce cell-mediated immune responses. We showed that our vaccine platform effectively stimulates a robust cellular immune response against protein S. Moreover, we confirmed that gp96-Ig, secreted from allogeneic cells expressing full-length protein S, generates powerful, protein S polyepitope-specific CD4+ and CD8+ T cell responses in both lung interstitium and airways. These findings were further strengthened by the observation that protein-S -specific CD8+ T cells were induced in human leukocyte antigen (HLA)-A2-02-01 transgenic mice thus providing encouraging translational data that the vaccine is likely to work in humans, in the context of SARS-CoV-2 antigen presentation.

immunology↗

bioRxiv2020

Perforin-2 limits pathogen proliferation at the maternal-fetal interface

Placental immune responses are highly regulated to strike a balance between protection and tolerance. For relatively mild infections, protection encompasses both the mother and fetus; however, during worsening conditions, protection becomes exclusively reserved for the mother. Previously, we and others have shown that the host factor Perforin-2 plays a central role in protecting mice and cells against infection. Here, we analyzed Perforin-2 activity in the mouse placenta to determine whether Perforin-2 plays a similarly protective role. We show that Perforin-2 is critical for inhibiting Listeria monocytogenes colonization of the placenta and fetus and that this protection is due to both maternal and fetal-encoded Perforin-2. Perforin-2 mRNA is readily detectable in individual immune cells of the decidua and these levels are further enhanced specifically in decidual macrophages during high-dose infections that result in fetal expulsion. Unexpectedly, inductive Perforin-2 expression in decidual macrophages did not occur during milder infections in which fetal viability remained intact. This pattern of expression significantly differed from that observed in splenic macrophages in which inductive Perforin-2 expression was observed in both high and mild infection conditions. In the placenta, inductive Perforin-2 expression in decidual macrophages was co-incident with their polarization from a M2 to M1 phenotype that normally occurs in the placenta during high-burden infections. Our results suggest that Perforin-2 is part of a host response that is protective either for both the mother and fetus in milder infections or exclusively for the mother during high-dose infections.

immunology↗