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Natarajan, B.

Publications and source records attributed to Natarajan, B..

4 recordsLinked to original sources

MicroRNA166-HD-ZIP III module impacts tuber shape, color and productivity in potato

Tuber shape and size are important traits in potato. Although several factors governing tuberization have been well studied, the molecular mechanisms regulating the tuber shape and size are still elusive. Here, we demonstrate that suppression of miR166, which targets class III HD-ZIP transcription factors, alters tuber morphology and productivity in potato. Target mimicry of miR166 (MIM166) in Solanum tuberosum ssp. Andigena resulted in elongated, pigmented tubers with reduced yield under short-day conditions. Transcriptome profiling of the tuberizing stolons - swollen head vs. stalk revealed differential expression of auxin-, cytokinin-, and gibberellin-associated genes, consistent with altered hormone levels. The coloured tubers from MIM166 line exhibited differential accumulation of cyanidin 3-glucoside, pelargonidin 3-glucoside, and delphinidin 3-glucoside. Tuber productivity in these lines was reduced possibly due to the decreased expression of SWEET11b and distorted vascular structures. Further, the miR166 target-StREVOLUTA exhibited dynamic expression during stolon-to-tuber transition, and could modulate StYUCCA7 expression, an auxin biosynthesis gene. Increased pigmentation and auxin accumulation in MIM166, reduced expression of auxin biosynthesis genes in REVOLUTA antisense, and low tuber yield collectively suggest miR166-REV as a regulatory module of auxin homeostasis in differentiating stolons that influences tuber morphology. These results reveal a previously unrecognized miRNA-mediated pathway governing storage organ shape, and extends the functional scope of the miR166-HD-ZIP III module beyond organ polarity. Significance statementLimited studies describe the molecular mechanisms regulating tuber shape in storage organ development. Here, we show that the miR166-REVOLUTA-auxin network has significant regulatory roles in potato development, influencing tuber shape, pigmentation, and productivity. These findings provide insights into molecular control of tuber morphology, uncover hitherto unknown functions of the miR166-REVOLUTA module in tuber crops, and broadens our understanding of miR166-mediated developmental regulation in plants.

plant biology↗

Exosomes are vehicles for the stress-regulated secretion of histones

Histones are conserved nuclear proteins that function as part of the nucleosome in the regulation of chromatin structure and gene expression. Interestingly, extracellular histones populate biofluids from healthy individuals and when elevated may contribute to various acute and chronic diseases. It is generally assumed that most extracellular histones exist as nucleosomes, as components of extracellular chromatin. We analysed cell culture models under normal and stressed conditions to identify pathways of histone secretion. We report that core and linker histones localize to extracellular vesicles (EVs) and are secreted via the multivesicular body/exosome pathway. Upregulation of histone EV secretion occurs in response to cellular stress, with enhanced vesicle secretion and a shift towards a population of smaller EVs. Most histones were membrane associated with the outer surface of EVs. Degradation of EV-DNA did not impact significantly on EV-histone association. Individual histones or histone octamers bound strongly to liposomes and EVs, but nucleosomes did not, showing histones do not require DNA for EV binding. EV histones colocalized most frequently with the tetraspanin CD63 but using genetic or pharmacological intervention, we found that all known pathways of exosome biogenesis acted positively on histone secretion. Inhibition of autophagy and lysosomal degradation had a strong positive effect on EV histone release. Unexpectedly, EV-associated histones lacked the extensive post-translational modification of their nuclear counterparts, suggesting loss of PTMs may be involved in their trafficking or secretion. Our data does not support a significant role for EV-histones existing as nucleosomes. We show for the first time that histones are secreted from cells as membrane proteins via EVs/exosomes. This fundamental discovery provides support for further investigation of the biological activity of exosome associated histones and their role in disease.

cell biology↗

Canonical and ETT-mediated auxin signalling pathways synergistically promote gynoecium development in Arabidopsis thaliana

Gynoecium polarity establishment is regulated by auxin, a phytohormone whose signal is transduced through several pathways. The relationship between the ETT and canonical TIR1/AFB pathways, and their relevance for carpel development beyond Arabidopsis thaliana, have not been investigated. The data presented here show that the expression patterns of canonical and ETT-mediated signalling components, and phenotypes of higher order mutants are shared between Arabidopsis and Capsella rubella. tir1 afb2 ett mutants partially phenocopy ett arf4 double mutants, suggesting a role for AUXIN RESPONSE FACTOR 4 (ARF4) in the integration of canonical and ETT-mediated signalling. Comparative transcriptomics revealed that the auxin-independent mis-regulation of YABBY genes correlate with patterning defects observed in Arabidopsis ett arf4 mutants. Together, the data presented suggest conserved synergism between canonical and ETT-mediated pathways in gynoecium polarity establishment in the Brassicaceae. Finally, the data suggest that ETT/ARF4 function to prevent the auxin-induced expression of a range of targets in Arabidopsis, consistent with activator-repressor ARF antagonism, and implying that the maintenance of auxin insensitivity by repressive ARFs is important for a range of biological processes. Summary StatementHere the relationship between canonical and ETT-mediated auxin signalling machineries is investigated in Arabidopsis and Capsella revealing conserved synergism between these two pathways in Brassicaceae with distinct fruit shapes.

plant biology↗

Hypoxia mediated regulation of mitochondrial transcription factors: Implications of hypertensive renal physiology

Kidneys have a high resting metabolic rate and low tissue partial pressure of oxygen due to enhanced mitochondrial oxygen consumption and ATP production for active solute transport. Enhanced mitochondrial activity leads to progressive hypoxia from the renal cortex to renal medulla. Renal tubulointerstitial hypoxia (TiH) is severe in hypertensive rats due to increased sodium reabsorption within their nephrons. Additionally, these rats display increased energy demand and therefore, require healthy mitochondria for adequate salt reabsorption. Hence, we sought to study the regulation of mitochondrial biogenesis and expression of mitochondrial transcription factors (mtTFs, viz. Tfam, Tfb1m and Tfb2m) during hypoxic conditions and in rodent models of genetic hypertension. We report that the expressions of HIF-1 (hypoxia inducible factor-1), PGC-1 (peroxisome proliferator activated receptor-{gamma} co-activator-1), mtTFs and OXPHOS proteins are elevated in hypertensive rats as compared to their normotensive counterparts. Additionally, studies in cultured kidney cells show that acute hypoxia augments the expression of these genes. We also observe a positive correlation between HIF-1 and mtTFs transcripts in human tissues. Furthermore, we report for the first time to our knowledge, that HIF-1 binds to promoters of Tfam, Tfb1m and Tfb2m genes and augments their promoter activities in NRK52e cells subjected to acute hypoxia. Taken together, this study suggests that acute hypoxia may enhance mitochondrial function to meet the energy demand in renal tubular epithelial cells and in young/pre-hypertensive SHR kidneys. Translational StatementOur results suggest that tubulointerstitial hypoxia (TiH) prevailing in prehypertensive rats augments the expression of mitochondrial transcription factors and proteins of electron transport chain. Moreover, previous reports indicate that ATP synthesis in these rats are elevated. Thus, our study provides insights into the molecular mechanism of such enhanced mitochondrial function. We propose that during early stages of kidney diseases (marked by mild TiH) an enhancement of mitochondrial function via stimulation of HIF-1/PGC-1 production may delay renal tubular damage.

molecular biology↗