Biology subjects

Tahir, J.

Publications and source records attributed to Tahir, J..

6 recordsLinked to original sources

bioRxiv2025

Defense-Suppressive Fragments of RIN4 generated by AvrRpt2 Participate in NDR1-dependent Activation of RPS2

Plant nucleotide-binding, leucine-rich-repeat (NLR) immune receptors recognize pathogen effectors and activate immunity. The NLR RPS2 recognizes AvrRpt2, a Pseudomonas effector that promotes virulence by proteolytically cleaving a membrane-tethered host protein, RIN4. RIN4 cleavage by AvrRpt2 generates fragments that activate RPS2. A model for RPS2 activation by RIN4 destruction is consistent with the ectopic activity of RPS2 in plants lacking RIN4 but does not explain the link between AvrRpt2s virulence activity and RPS2 activation. We found that non-membrane-tethered RIN4 derivatives are potent cytosolic activators of RPS2. Activation of RPS2 by these RIN4 derivatives, like AvrRpt2-induced activation, and unlike ectopic activation in the absence of RIN4, requires the defense signaling protein NDR1. Cleavage products of RIN4 produced by AvrRpt2 play contrasting roles in the activation of RPS2, with the membrane-tethered C-terminal fragment suppressing RPS2 and the non-membrane-tethered internal fragment, dependent on compatibility with the C-terminal fragment, overcoming its suppression of RPS2. HighlightsO_LINon-membrane tethered derivatives of RIN4 activate RPS2-induced cell death C_LIO_LIActivation of RPS2 by non-membrane-tethered derivatives of RIN4 requires NDR1 C_LIO_LIAvrRpt2-induced cleavage fragments of RIN4 play contrasting roles in RPS2 activation C_LI

plant biology↗

bioRxiv2024

Identification and characterization of innate immunity in Actinidia melanandra in response to Pseudomonas syringae pv. actinidiae

Pseudomonas syringae pv. actinidiae biovar 3 (Psa3) has decimated kiwifruit orchards growing susceptible kiwifruit Actinidia chinensis varieties. Effector loss has occurred recently in Psa3 isolates from resistant kiwifruit germplasm, resulting in strains capable of partially overcoming resistance present in kiwiberry vines (A. arguta, A. polygama, and A. melanandra). Diploid male A. melanandra recognises several effectors, sharing recognition of at least one avirulence effector (HopAW1a) with previously studied tetraploid kiwiberry vines. Sequencing and assembly of the A. melanandra genome enabled the characterisation of the transcriptomic response of this non-host to wild-type and genetic mutants of Psa3. A. melanandra appears to mount a classic effector-triggered immunity (ETI) response to wildtype Psa3 V-13, as expected. Surprisingly, the type III secretion (T3S) system-lacking Psa3 V-13 {Delta}hrcC strain did not appear to trigger pattern-triggered immunity (PTI) despite lacking the ability to deliver immunity-suppressing effectors. Contrasting the A. melanandra responses to an effectorless Psa3 V-13 {Delta}33E strain and to Psa3 V-13 {Delta}hrcC suggested that PTI triggered by Psa3 V-13 was based on the recognition of the T3S itself. The characterisation of both ETI and PTI branches of innate immunity responses within A. melanandra further enables breeding for durable resistance in future kiwifruit cultivars.

plant biology↗

bioRxiv2022

Contrasting effector profiles between bacterial colonisers of kiwifruit reveal redundant roles and interplay converging on PTI-suppression and RIN4

O_LITesting effector-knockout strains of the Pseudomonas syringae pv. actinidiae biovar 3 (Psa3) for reduced in planta growth in their native kiwifruit host revealed a number of non- redundant effectors that contribute to Psa3 pathogenicity. Conversely, complementation in the weak kiwifruit pathogen P. syringae pv. actinidifoliorum (Pfm) for increased growth identified redundant Psa3 effectors. C_LIO_LIPsa3 effectors hopAZ1a and HopS2b and the entire exchangeable effector locus ({Delta}EEL; 10 effectors) were significant contributors to bacterial colonisation of the host and were additive in their effects on pathogenicity. Four of the EEL effectors (HopD1a, AvrB2b, HopAW1a, and HopD2a) redundantly contribute to pathogenicity through suppression of pattern-triggered immunity (PTI). C_LIO_LIImportant Psa3 effectors include several redundantly required effectors early in the infection process (HopZ5a, HopH1a, AvrPto1b, AvrRpm1a, and HopF1e). These largely target the plant immunity hub, RIN4. C_LIO_LIThis comprehensive effector profiling revealed that Psa3 carries robust effector redundancy for a large portion of its effectors, covering a few functions critical to disease. C_LI

plant biology↗

bioRxiv2021

Switch-like and persistent memory formation in individual larval Drosophila

Associative learning allows animals to use past experience to predict future events. The circuits underlying memory formation support immediate and sustained changes in function, often in response to a single example. Larval Drosophila is a genetic model for memory formation that can be accessed at molecular, synaptic, cellular, and circuit levels, often simultaneously, but existing behavioral assays for larval learning and memory do not address individual animals, and it has been difficult to form long lasting memories, especially those requiring synaptic re-organization. We demonstrate a new assay for learning and memory capable of tracking the changing preferences of individual larvae. We use this assay to explore how activation of a pair of reward neurons changes the response to the innately aversive gas Carbon Dioxide (CO2). We confirm that when coupled to odor presentation in appropriate temporal sequence, optogenetic reward reduces avoidance of CO2. We find that learning is switch-like: all-or-none and quantized in two states. Memories can be extinguished by repeated unrewarded exposure to CO2 but are stabilized against extinction by repeated training or overnight consolidation. Finally, we demonstrate long-lasting protein synthesis dependent and independent memory formation.

neuroscience↗

bioRxiv2020

Agro-morphological, yield, and genotyping-by-sequencing data of selected wheat germplasm

Wheat (Triticum aestivum) is the most important staple food in Pakistan. Knowledge of its genetic diversity is critical for designing effective crop breeding programs. Here we report agro-morphological and yield data for 112 genotypes (including 7 duplicates) of wheat (Triticum aestivum) cultivars, advance lines, landraces and wild relatives, collected from several research institutes and breeders across Pakistan. We also report genotyping-by-sequencing (GBS) data for a selected sub-set of 52 genotypes. Sequencing was performed using Illumina HiSeq 2500 platform using the PE150 run. Data generated per sample ranged from 1.01 to 2.5 Gb; 90% of the short reads exhibited quality scores above 99.9%. TGACv1 wheat genome was used as a reference to map short reads from individual genotypes and to filter single nucleotide polymorphic loci (SNPs). On average, 364,074{+/-}54479 SNPs per genotype were recorded. The sequencing data has been submitted to the SRA database of NCBI (accession number SRP179096). The agro-morphological and yield data, along with the sequence data and SNPs will be invaluable resources for wheat breeding programs in future.

genetics↗

bioRxiv2019

Multiple quantitative trait loci contribute tolerance to bacterial canker incited by Pseudomonas syringae pv. actinidiae in kiwifruit (Actinidia chinensis)

Pseudomonas syringae pv. actinidiae (Psa) Biovar 3, a virulent, canker-inducing pathogen is an economic threat to the kiwifruit (Actinidia spp.) industry worldwide. The commercially grown diploid (2x) A. chinensis var. chinensis is more susceptible to Psa than tetraploid and hexaploid kiwifruit. However information on the genetic loci modulating Psa resistance in kiwifruit is not available. Here we report mapping of quantitative trait loci (QTLs) regulating tolerance to Psa in a diploid kiwifruit population, derived from a cross between an elite Psa-susceptible Hort16A and a tolerant male breeding parent P1. Using high-density genetic maps and intensive phenotyping, we identified a single QTL for Psa tolerance on Linkage Group (LG) 27 of Hort16A revealing 16-19% phenotypic variance and candidate alleles for susceptibility and tolerance at this loci. In addition, six minor QTLs were identified in P1 on distinct LGs, exerting 4-9% variance. Complete tolerance in the F1 population is attained by additive effects from Hort16A and P1 QTLs providing evidence that divergent genetic pathways fend-off virulent Psa strain. Two different bioassays further identified new QTLs for tissue-specific responses to Psa. Transcriptome analysis of Psa-tolerant and susceptible genotypes in field revealed hallmarks of basal defense and provided candidate RNA-biomarkers for screening Psa tolerance.

plant biology↗