Biology subjects

Maulana, M. I.

Publications and source records attributed to Maulana, M. I..

3 recordsLinked to original sources

bioRxiv2025

THE ROOT-KNOT NEMATODE EFFECTOR MJ-MSP18: A SWISS ARMY KNIFE FOR REPROGRAMMING PLANT IMMUNITY

Root-knot nematodes (Meloidogyne spp.) are obligatory plant root parasites whose effector proteins play a critical role in suppressing plant immunity. However, the effectors direct host targets and underlying molecular mechanisms remain poorly understood. Using TurboID-mediated proximity labeling in tomato (Solanum lycopersicum) hairy roots, we identified an interaction between the nematode effector Mj-MSP18 and the tomato BRASSINOSTEROID-SIGNALING KINASE 7 (Sl-BSK7). Yeast two-hybrid (Y2H) assays confirmed that this interaction is conserved in Arabidopsis thaliana and Nicotiana benthamiana. Additionally, yeast three-hybrid and luciferase complementation assays demonstrated that Mj-MSP18 disrupts the interaction between BSK7/8 and FLS2 in both yeast and in planta. Given that the BSK7/8-FLS2 interaction is essential for flg22-induced pattern-triggered immunity (PTI), this disruption likely accounts for the suppression of reactive oxygen species (ROS) production and callose deposition observed upon transient expression of Mj-MSP18 in flg22-treated N. benthamiana leaves. Correspondingly, Arabidopsis and tomato bsk7 mutants exhibited increased susceptibility to root-knot nematode infection. Furthermore, RNA-seq analysis of tomato hairy roots expressing Mj-MSP18 revealed extensive transcriptional reprogramming, including the downregulation of defence-related genes and hydrogen peroxide response pathways. In addition, Y2H screening identified Sl-MYB and Sl-MYC2 as additional interactors, linking Mj-MSP18 to phytohormone biosynthesis, particularly the brassinosteroid (BR) and salicylic acid (SA) pathways, as validated by targeted metabolite analysis. The conservation of Mj-MSP18 across Meloidogyne species suggests a broadly conserved mechanism for host immune suppression and phytohormone modulation.

plant biology↗

bioRxiv2025

A Chromosome-scale Reference Genome of Meloidogyne hapla reveals localized recombination hotspots enriched with Effector Proteins

Root-knot nematodes (Meloidogyne spp.) are among the most destructive agricultural pests that cause significant yield losses across a wide range of crops. Meloidogyne hapla, a diploid species, is a valuable model for studying root-knot nematodes due to its parasitic diversity, small genome, and a reproductive strategy that facilitates genetic analysis. Here, we present a high-quality chromosome-scale assembly of M. hapla, generated using multiple sequencing platforms-PacBio HiFi, ONT, Illumina and HiC. The 59 Mb assembly comprises 16 chromosome-length scaffolds, notably lacking canonical telomeric repeats. Instead, we identified a tandem 16-mer repeat mainly present at scaffold ends, suggesting an alternative system for chromosome-end maintenance. Genetic linkage analysis of F2 populations derived from crosses between M. hapla strains validated the assembly but also revealed anomalies indicating chromosome structure differences between parental isolates such as fissions, fusions, and rearrangements. This analysis also revealed sharply delineated zones of high recombination on most chromosome arms. We also identified 1,258 genes encoding putative secreted proteins (PSP), which should be enriched in genes involved in host interaction and pathogenicity. Most of the PSP genes had orthologs in other plant parasitic nematode species, and the majority were pioneers, lacking known functional domains. Notably, we found that PSPs are significantly enriched in high-recombination zones, possibly facilitating their rapid evolution. Overall, our study provides new insights into the genome structure of diploid root-knot nematodes and highlights the interplay between genome architecture, recombination, and parasitism. These findings raise new questions about how genetic and genomic adaptations drive the success of rootknot nematodes as plant parasites.

plant biology↗

bioRxiv2021

The genetic architecture underlying body-size traits plasticity over different temperatures and developmental stages in Caenorhabditis elegans

Most ectotherms obey the temperature-size rule, meaning they grow larger in a colder environment. This raises the question of how the interplay between genes and temperature affect the body size of ectotherms. Despite the growing body of literature on the physiological life-history and molecular genetic mechanism underlying the temperature-size rule, the overall genetic architecture orchestrating this complex phenotype is not yet fully understood. One approach to identify genetic regulators of complex phenotypes is Quantitative Trait Locus (QTL) mapping. Here, we explore the genetic architecture of body size phenotypes, and plasticity of body-size phenotypes in different temperatures using Caenorhabditis elegans as a model ectotherm. We used 40 recombinant inbred lines (RILs) derived from N2 and CB4856, which were reared at four different temperatures (16{degrees}C, 20{degrees}C, 24{degrees}C, and 26{degrees}C) and measured at two developmental stages (L4 and adult). The animals were measured for body length, width at vulva, body volume, length/width ratio, and seven other body-size traits. The genetically diverse RILs varied in their body-size phenotypes with heritabilities ranging from 0.0 to 0.99. We detected 18 QTL underlying the body-size traits across all treatment combinations, with the majority clustering on Chromosome X. We hypothesize that the Chromosome X QTL could result from a known pleiotropic regulator - npr-1 - known to affect the body size of C. elegans through behavioral changes. We also found five plasticity QTL of body-size which three of them colocalized with some body-size QTL at certain temperature. In conclusion, our findings shed more light on multiple loci affecting body size plasticity and the possibility of co-regulation of traits and traits plasticity by the same loci under different environment.

genetics↗