Biology subjects

Harshith, C. Y.

Publications and source records attributed to Harshith, C. Y..

5 recordsLinked to original sources

bioRxiv2025

Disulfide bond sculpts a peptide fold that mediates phytocytokine recognition

Precise ligand recognition by closely related leucine-rich repeat receptor kinases (LRR-RKs) is essential for plants to coordinate immunity, development, and environmental adaptation. Here, we show how HAESA-LIKE 3 (HSL3) specifically recognizes the folded, disulfide-stabilized CTNIP/SCREW phytocytokines in Arabidopsis. Quantitative binding assays define a minimal CTNIP4 region required for high-affinity HSL3 interaction and signaling activation. A 2.12 [A] crystal structure of the HSL3-CTNIP4 complex reveals a unique C-terminal receptor pocket that accommodates the peptides cyclic architecture through a combination of hydrophobic and polar contacts, a feature absent in the closely related HAE/HSL LRR-RKs. The cyclic CTNIP4 fold further establishes a largely hydrophobic interface that bridges HSL3 to the SERK co-receptor, forming a distinct activation surface. Together, these structural, biochemical and physiological insights uncover a previously unrecognised mechanism of peptide perception and receptor activation, highlighting how subtle architectural variations enable precise ligand selectivity among highly conserved plant receptor kinases.

plant biology↗

bioRxiv2025

Copper-sensitive OsSPL9 TF regulates expression of indica rice domestication-associated miRNAs and phenotypes

Domestication of indica rice facilitated better harvest and yield, however the molecular mechanisms that drove multitude of the associated phenotypes is poorly understood. A few genetic and epigenetic mechanisms have been attributed to indica rice domestication; however, upstream regulators of these variations are unknown. Here, we identified a copper (Cu)-dependent regulatory module, involved in the regulation of OsSPL9 TF and two classes of RNAs under its control. Differential accumulation of Cu-associated micro(mi)RNAs and Cu-associated protein-coding RNAs were a major portion of the differences between wild (Oryza nivara) and cultivated rice lines. We identified OsSPL9 as an upstream regulator of these changes through genetic and molecular analysis as well as by using Cu stressed conditions. OsSPL9 bound to the promoters of these genes through a conserved GTAC enriched motif. OsSPL9, Cu-associated miRNAs and their targets acted as a regulatory loop, since mis-expression of SPL9 alone, or any individual Cu-associated miRNA, also altered levels of other Cu-miRNAs and their cognate targets. OsSPL9-mediated regulation was closely linked to Cu accumulation and metabolism, indicating previously unappreciated roles of metal ions in mediating domestication-associated phenotypes. Our study facilitates a better understanding of the crosstalk between genetic and epigenetic regulation that contributed to indica rice domestication.

plant biology↗

bioRxiv2025

OsWRKY53 dictates wound responses in rice through fine-tuning cross-talk between PEP and PSK mediated signalling

Wounding and tissue damage are major events among the multitude of stresses that plants face in their natural environment. Wound response is a very dynamic event that involves the integration of various regulatory networks culminating in successful wound-induced downstream signalling. Plants depend on endogenously derived molecular signals to initiate wound responses. Transcriptional response is paramount in dictating successful transition of early defense to late growth responses. Here we show the involvement of a WRKY transcription factor (TF) named OsWRKY53, that is responsive to both wounding as well as wound-derived plant elicitor peptide (PEP), OsPep2 treatments. OsWRKY53 is involved in positive regulation of gene expression of OsPep2 responsive genes. OsWRKY53 displays altered DNA occupancy in response to OsPep2 treatment over time correlating with the altered gene expression. Further, OsWRKY53 is involved in simultaneous activation and suppression of OsPep2-responsive and phytosulfokine (PSK) responsive genes, respectively. In agreement with these, mis-expression of OsWRKY53 led to compromised wound responses. Collectively, we establish that OsWRKY53 acts at the intersection of PEP and PSK mediated transition of wound responses and positively regulates the early defense-related gene expression.

plant biology↗

bioRxiv2023

Wound induced small-peptide mediated signalling cascade regulated by OsPSKR, dictates balance between growth and defense in rice

Wounding is a general stress in plants that results from various pest and pathogenic infections in addition to environment induced mechanical damages. Plants have sophisticated molecular mechanisms to recognize and respond to pests and pathogens. Although several molecules such as phytohormones, peptides and receptors have been attributed to wound responses in dicots, such mechanisms for monocots probably having distinct wound responses are less understood. Here, we show the involvement of two distinct categories of temporally separated, endogenously derived peptides, namely, plant elicitor peptides (PEPs) and phytosulfokine (PSK), that mediate wound responses in rice. These peptides trigger a dynamic signal relay in which a novel receptor kinase named OsPSKR played a major role. OsPSKR perceived PSK ligand, acting in association with a co-receptor OsSERK1, to activate downstream responses in a kinase activity-dependent manner. Perturbation of OsPSKR expression in rice led to compromised development and constitutive autoimmune phenotypes. These results suggested that OsPSKR maintains the trade-off between growth and exaggerated defense responses, both during homeostasis and wounding. Collectively, these findings indicate the presence of a stepwise peptide-mediated signal relay that regulates the transition from defense to growth upon wounding in monocots. One line summaryEndogenous peptide signalling initiated wound responses through a receptor-like kinase OsPSKR to maintain the balance between growth and defense responses.

plant biology↗

bioRxiv2021

Geminiviral βC1 orchestrates organellar genomic instability to augment viral infection by hijacking host RecA

Chloroplast is the site for transforming light energy to chemical energy. It also acts as a production unit for a variety of defense-related molecules. These defense moieties are necessary to mount a successful counter defence against pathogens including viruses. Geminiviruses disrupt chloroplast homeostasis as a basic strategy for their successful infection inducing vein-clearing, mosaics and chlorosis in infected plants. Here we show that a geminiviral pathogenicity determinant protein {beta}C1 directly interferes with plastid homeostasis. {beta}C1 was capable of inducing organelle-specific nuclease to degrade plastid genome as well as diverted functions of RecA1 protein, a major player in plastid genome maintenance. {beta}C1 interacted with RecA1 in plants and its homolog in bacteria to reduce the ability of host cells to maintain genomic integrity under stresses. Further, reduction in the coding capacity of plastids severely affected retrograde signalling necessary for viral perception and activation of defense. Induction of chloroplast-specific nuclease by {beta}C1 is similar to phosphate starvation-response in which nucleotides are recycled to augment synthesis of new, potentially viral, DNA. These results indicate the presence of a novel strategy in which a viral protein alters host defence by targeting regulators of chloroplast DNA. We predict that the mechanism identified here might have similarities in other plant-pathogen interactions. One line summary{beta}C1 alters plastid genome metabolism.

plant biology↗