Biology subjects

Lara, A.

Publications and source records attributed to Lara, A..

3 recordsLinked to original sources

bioRxiv2026

SlCIPK26 enhances tomato fertility by activating the K+ transporter SlHAK5 in reproductive tissues

In tomato plants, the potassium (K) transporter SlHAK5 is integral to root K uptake and overall plant fertility. Under K deficiency, SlHAK5 expression is induced in roots and the encoded transporter is activated via the Ca{superscript 2}-sensing CIPK/CBL complex SlCIPK23/SlCBL1-9. In Arabidopsis, multiple CIPK/CBL complexes can activate AtHAK5, providing alternative regulatory pathways that enhance K uptake. However, the architecture of CIPK/CBL signaling networks has diverged among plant species, necessitating species-specific identification of novel regulatory components. Accordingly, we screened additional tomato CIPK proteins for their capacity to modulate SlHAK5 activity in yeast. SlCIPK15 and SlCIPK26 emerged as potent activators of SlHAK5, acting in concert with SlCBL9. Functional characterization of slcipk15 and slcipk26 mutants revealed that neither contributed significantly to SlHAK5-mediated K uptake in roots. Conversely, both mutants exhibited impaired pollen tube elongation, correlating with reduced K content in pollen relative to wild type. Notably, slcipk26 mutants displayed more severe pollen defects, phenocopying the slhak5 mutant. Further analyses demonstrated that slcipk26 plants suffered compromised seed set and pistil function, paralleling the reproductive deficiencies observed in slhak5 mutants. These findings implicate SlCIPK26 as the principal regulator of SlHAK5 in reproductive tissues. Collectively, our data underscore the role of CIPK paralogs in orchestrating tissue-specific regulation of target proteins, thereby enabling fine-tuned modulation of K transport essential for both vegetative and reproductive development.

plant biology↗

bioRxiv2019

Early vegetation recovery after the 2008-2009 explosive eruption of the Chaiten Volcano

In May 2008, Chaiten volcano entered in eruptive process, one of the world largest eruptions in the last decades. The catastrophic event left different type of disturbance and caused diverse environmental damage distributed heterogeneously in the surrounding areas of the volcano. We went to the field to assess the early vegetation responses a year after the eruption, in September 2009. Particularly, we evaluated the lateral-blast disturbance zone. We distributed a set of plots in three disturbed sites, and one in an undisturbed site. In each of these sites, in a plot of 1000m2 we marked all stand tree, recording whether they were alive, resprouting or dead. Additionally, in each site 80 small-plots (~4m2) we tallied the plants regeneration, its coverage, and the log-volume. We described whether the plant regeneration was growing on mineral or organic substrate. In the blast-zone the eruption created a gradient of disturbance. Close to the crater we found high devastation marked by no surviving species, scarce standing-dead trees and logs, as well as no tree regeneration. On the other extreme of the disturbance gradient, the trees with damaged crown were resprouting, small-plants were regrowing and seedlings were more dispersed. The main regeneration strategy was the resprouting of trunks or buried roots, while few seedlings were observed in the small plots and elsewhere in disturbed areas. However, the assessment was too soon after the eruption and updated monitoring is required to confirm observed patterns. The main findings of this study are: i) a mosaic of pioneering-wind dispersed species, scattered survivors regrowing and spreading from biological legacies, and plant species dispersed by frugivorous birds, likely favored by the biological legacies; (ii) the early succession is influenced by the interaction of the species-specific life history, altitudinal gradient and the different intensity of disturbance.

ecology↗

bioRxiv2018

Clinical Characterization of Host Response to Simian Hemorrhagic Fever Virus Infection in Permissive and Refractory Hosts: A Model for Determining Mechanisms of VHF Pathogenesis

Simian hemorrhagic fever virus (SHFV) causes a fulminant and typically lethal viral hemorrhagic fever (VHF) in macaques (Cercopithecinae: Macaca spp.) but causes subclinical infections in patas monkeys (Cercopithecinae: Erythrocebus patas). This difference in disease course offers a unique opportunity to compare host-responses to infection by a VHF-causing virus in biologically similar susceptible and refractory animals. Patas and rhesus monkeys were inoculated side-by-side with SHFV. In contrast to the severe disease observed in rhesus monkeys, patas monkeys developed a limited clinical disease characterized by changes in complete blood counts, serum chemistries, and development of lymphadenopathy. Viremia was measurable 2 days after exposure and its duration varied by species. Infectious virus was detected in terminal tissues of both patas and rhesus monkeys. Varying degrees of overlap in changes in serum concentrations of IFN-{gamma}, MCP-1, and IL-6 were observed between patas and rhesus monkeys, suggesting the presence of common and species-specific cytokine responses to infection. Similarly, quantitative immunohistochemistry of terminal livers and whole blood flow cytometry revealed varying degrees of overlap in changes in macrophages, natural killer cells, and T-cells. The unexpected degree of overlap in host-response suggests that relatively small subsets of a hosts response to infection may be responsible for driving pathogenesis that results in a hemorrhagic fever. Furthermore, comparative SHFV infection in patas and rhesus monkeys offers an experimental model to characterize host-response mechanisms associated with viral hemorrhagic fever and evaluate pan-viral hemorrhagic fever countermeasures.\n\nIMPORTANCEHost-response mechanisms involved in pathogenesis of VHFs remain poorly understood. An underlying challenge is separating beneficial, inconsequential, and detrimental host-responses during infection. The comparison of host-responses to infection with the same virus in biologically similar animals that have drastically different disease manifestations allows for the identification of pathogenic mechanisms. SHFV, a surrogate virus for human VHF-causing viruses likely causes subclinical infection in African monkeys such as patas monkeys but can cause severe disease in Asian macaque monkeys. Data from the accompanying article by Buechler et al. support that infection of macaques and baboons with non-SHFV simarteviruses can establish persistent or long-term subclinical infections. Baboons, macaques, and patas monkeys are relatively closely taxonomically related (Cercopithecidae: Cercopithecinae) and therefore offer a unique opportunity to dissect how host-response differences determine disease outcome in VHFs.

immunology↗