Biology subjects

Nair, A. M.

Publications and source records attributed to Nair, A. M..

6 recordsLinked to original sources

bioRxiv2026

The systemically induced sugar transporter SWEET11 regulates growth-defense trade-offs during Serendipita indica symbiosis in Arabidopsis

Sugar exchange at the root interface is a pivotal process governing the establishment and stability of plant-fungal symbioses. Precise regulation of sugar exchange determines the success of this ecologically significant interaction. Sugar Will Eventually be Exported proteins (SWEETs) constitute a family of regulatory, energy-independent bidirectional sugar transporters that influence plant development, stress resilience, and survival. However, how specific SWEET transporters coordinate systemic carbon allocation and immune regulation during beneficial plant-fungal interactions remains poorly understood. In this study, we examined the role of the systemically induced Arabidopsis sugar transporter SWEET11 during association with the beneficial endophytic fungus Serendipita indica and following treatment with its elicitor, cellotriose (CT). Expression profiling of SWEET family members revealed a rapid and preferential induction of SWEET11 in aerial tissues upon fungal colonization and CT treatment. Loss-of-function of SWEET11 compromises key mutualistic outcomes, including plant growth enhancement, fungal colonization efficiency, penetration ability, carbohydrate distribution, and the regulation of defense-related phytohormones such as jasmonic acid and abscisic acid. Global transcriptome analysis further demonstrated that SWEET11 regulates whole-plant responses by orchestrating genes involved in central metabolism, secondary metabolite production, sesquiterpenoid and triterpenoid pathways, as well as defense signaling and nutrient transport systems. We show that SWEET11 interacts with a stress associated SNF1-related protein kinase (SnRK2.8) and plays a crucial role in enabling fungal establishment while mitigating host defense responses, and supporting plant growth. Our data shows that SWEET11 functions as a shoot-derived sugar exporter that directs carbon toward roots, facilitating sugar unloading to S. indica. This controlled carbon supply allows the fungus to meet its metabolic demands without disrupting host sugar balance, thereby maintaining a stable and well-regulated symbiotic association under immune constraints.

plant biology↗

bioRxiv2025

SARS-CoV-2 infection induced alterations in ADAR editing patterns differ between patients who developed critical compared to non-critical COVID-19

COVID-19, caused by the SARS-CoV-2 virus, has a wide spectrum of clinical presentations even among individuals with similar demographics. Disease severity has been linked with viral recognition-triggered expression of Interferons (IFNs) and Interferon stimulated genes (ISGs). Among these ISGs, ADARp150 is a member of adenosine deaminases acting on RNA (ADARs) enzyme family. ADARs are RNA editing enzymes that contribute to transcriptome diversity and modulate immune response during viral infections. While previous studies have identified altered ADAR expression and editing patterns during SARS-CoV-2 infection, it remains unknown whether ADAR expression and activity differ between patients with varying severities of COVID-19, specifically, in individuals who developed critical compared to non-critical COVID-19. We address this question by analyzing a publicly available, deeply sequenced whole blood RNA-seq dataset from individuals with either critical or non-critical COVID-19, matched for age, sex, and presence of comorbidities. Our results show differential expression of thousands of genes, including those involved in neutrophil degranulation, and upregulation of ADAR1 and its isoform ADARp110 in patients with critical COVID-19. We further identify global differences in the total number of edits, driven by ADAR1 and ADAR2 expression levels in critical but not in non-critical patients. ADAR activity also differed within Alu elements and in the proportion of edits with varying functional consequences. We further identified severity specific editing events, including nonsynonymous edits, within distinct biological pathways. Moreover, we identified 140 high confidence editing sites within 126 genes, that are differentially edited between the two patient groups. These genes were enriched in infectious disease, cell cycle, signal transduction, RNA and protein metabolism in addition to inflammatory pathways such as neutrophil degranulation and signaling by interleukins. Enrichment/modulation of neutrophil degranulation pathway at transcriptional and post transcriptional levels suggest the importance, complex regulation, and contribution of this pathway in COVID-19 disease severity. Finally, using a random forest classifier, we identified a set of differentially edited sites that could serve as molecular markers for COVID-19 disease severity. Together, our study demonstrates varying expression and editing patterns of ADARs between critical and non-critical patients, suggesting a potential role of ADAR editing in varying severity of COVID-19 pathogenesis.

bioinformatics↗

bioRxiv2025

Arabidopsis SWEET12 regulates sugar allocation and defense responses to sustain beneficial association with Serendipita indica in roots

Carbon availability is a central determinant of beneficial plant-fungal associations, and sugar transporters are key levers of this exchange. SWEETs (SUGARS WILL EVENTUALLY BE EXPORTED TRANSPORTER) are involved in transporting various kinds of sugars in plants; however, their functional roles in fungal symbiosis are not sufficiently explored. In this study, we investigate the functional relevance of Arabidopsis SWEETs in the interaction with endophytic fungi, Serendipita indica. Transcript profiling of SWEET genes in response to S. indica and its major elicitor, cellotriose, revealed early root-specific induction of SWEET12. Using a SWEET12 loss-of-function mutant, we demonstrate that the absence of SWEET12 disrupts the major outcomes of mutualism including growth promotion, balanced colonization, sugar allocation, and the accumulation of defense phytohormones (JA and SA). Transcriptome profiling further reveals that SWEET12 buffers whole-plant responses by coordinating genes linked to carbohydrate, nitrogen, and lipid metabolism, and by tuning defense signalling and nutrient transporter networks. Our findings indicate that SWEET12 is essential for balancing fungal colonization and host defense, thereby promoting plant growth. SWEET12 does so by acting as sugar valve that meters sugar release to the apoplast, enabling the fungus to access carbon while preserving host sugar homeostasis and immune competence.

plant biology↗

bioRxiv2025

SARS-CoV-2-induced dysregulation in ADAR editing patterns persists post viral clearance in individuals with mild COVID-19

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections remain a public health concern worldwide. Viral antigen triggered innate immune response leads to induction of interferons (IFNs) and interferon stimulated genes (ISGs) including ADAR1 p150 isoform, which edits adenosine (A) residues within double stranded RNAs in both the virus and the host. Such RNA editing mediated by ADARs plays a crucial role in innate immune responses during viral infections through modulation of host-virus interactions. Additionally, ADAR editing acts post-transcriptionally, and serves as a mechanism of dynamic regulation of transcriptome and proteome diversity. While evidence points to changes in ADAR editing during infection, we do not know whether editing targets change over the course of the infection. Here, we explored temporal changes in ADAR expression and editing patterns, across three distinct stages of SARS-CoV-2 infection. Furthermore, we examined whether infection-triggered dysregulation in ADAR editing persists or returns to pre-infection states post-viral clearance. We addressed this question by analyzing publicly available whole blood RNA sequencing samples from forty-five, age-matched individuals. The individuals selected had no documented comorbidities, developed mild COVID-19, and were sampled across three distinct stages of SARS-CoV-2 infection: pre-, mid-, and post-infection. Our results demonstrate dynamic changes in ADAR expression and editing across the three stages. We further identified unique editing sites resulting from SARS-CoV-2 infection, across all three stages of infection, within genes involved in immune response pathways. Noteworthy, genes within neutrophil degranulation pathway appear to be edited, suggesting they may play a role in inflammation and sequelae observed post-SARS-CoV-2 infection. Our results demonstrate a consistent trend of elevated ADAR expression and reduced overall ADAR editing within each individual mid-infection. Subsequently, in some post-infection samples ADAR expression returns to approximately pre-infection levels, while in others it remains dysregulated. These differences may be contributing to heterogeneity in disease outcomes seen in individuals post-SARS-CoV-2 infection.

bioinformatics↗

bioRxiv2024

The role of ADAR editing and nonsense-mediated decay in Parkinson's Disease

Parkinsons Disease (PD) is a multifactorial disease with heterogenous phenotypes that vary across individuals, as well as by age and sex. Therefore, it is likely that multiple interacting factors, such as environmental influences and aging, as well as genetic factors, including dynamic RNA (ADAR, Adenosine Deaminases Acting on RNA) editing, may play a role in PD pathology. In this analysis of 317 transcriptomes of healthy controls, PD and prodromal patients aged 65 years or older, from Parkinsons Project Markers Initiative dataset, we observe differences in ADAR expression, number of putative ADAR edits, editing index, and the number of high and moderate impact edits between control groups and diseased samples, particularly when ADAR editing is associated with nonsense-mediated decay (NMD). Likewise, differentially expressed genes between comparison groups were linked to NMD-related pathways. NMD is an important process in detecting deleterious nonsense sequences in mRNA transcripts and eliminating them from the cell. Thus, NMD regulation serves an important role in neurodevelopment, neural differentiation, and neural maturation. RNA misprocessing, which includes dysregulation of NMD, is known to play an important role in neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) and fronto-temporal dementia. Our results suggest that NMD may also be an important factor in PD physiology.

bioinformatics↗

bioRxiv2023

Alterations in RNA editing in skeletal muscle following exercise training in individuals with Parkinsons disease

Parkinsons Disease (PD) is the second most common neurodegenerative disease behind Alzheimers Disease, currently affecting more than 10 million people worldwide and 1.5 times more males than females. The progression of PD results in the loss of function due to neurodegeneration and neuroinflammation. The etiology of PD is multifactorial, including both genetic and environmental origins. Here we explored changes in RNA editing, specifically editing through the actions of the Adenosine Deaminases Acting on RNA (ADARs), in the progression of PD. Analysis of ADAR editing of skeletal muscle transcriptomes from PD patients and controls, including those that engaged in a rehabilitative exercise training program revealed significant differences in ADAR editing patterns based on age, disease status, and following rehabilitative exercise. Further, deleterious editing events in protein coding regions were identified in multiple genes with known associations to PD pathogenesis. Our findings of differential ADAR editing complement findings of changes in transcriptional network identified by a recent Lavin et al. (2020) study and offer insights into dynamic ADAR editing changes associated with PD pathogenesis.

bioinformatics↗