Project description:Multiple herbicide resistance in Palmer amaranth (Amaranthus palmeri S. Watson) poses a serious threat to US crop production. A Palmer amaranth population (KCTR) from Kansas was found resistant to herbicides across six sites of action, including ALS-, PS II-, EPSPS-, PPO-, HPPD-inhibitors and synthetic auxins. Moreover, a predominance of metabolic resistance, possibly mediated by P450s or GSTs enzyme activity was reported in this population. This study aims to identify the specific genes involved in multiple herbicide metabolism in this Palmer amaranth population via transcriptome analysis. Vegetative clones were developed from three biological replicates of both resistant (KCTR/KCTR-G2) and susceptible (KSS) Palmer amaranth populations. Ten to 12 cm tall clones from each biological replicate were treated with labelled doses of chlorsulfuron, 2,4-D, atrazine, lactofen and mesotrione. Leaf samples were collected for RNA isolation at 6 hours after treatment with respective herbicides along with non-treated plants. Upon RNA sequencing, paired end reads generated were mapped to the Palmer amaranth transcriptome using HISAT2. Differential gene expression analysis revealed 414, 129, 529, 688 and 152 genes expressed differentially in resistant plants following chlorsulfuron, 2,4-D, atrazine, lactofen and mesotrione treatments, respectively. Isoforms of CYP72A219 or CYP704B1 and GST C-terminal were alternatively up-regulated expression across treatments. Transcripts for CYP72A219 and CYP704B1 show up-regulated expression of 3.4- to 6.6-fold and 5.9- to 12.4-fold in resistant plants as validated by qRT-PCR. Identification of genes involved in multiple herbicide metabolism in Palmer amaranth is crucial to predict the evolutionary course of herbicide resistance in weed species.
Project description:RNA-binding proteins and messenger RNAs assemble into ribonucleoprotein granules that regulate mRNA trafficking, local translation, and turnover. The dysregulation of RNA-protein condensation disturbs synaptic plasticity and neuron survival, and has been widely associated with human neurological disease. Neuronal granules are thought to condense around particular proteins that dictate the identity and composition of each granule type. Here, we show in Drosophila that a previously uncharacterized long non-coding RNA, mimi, is required to scaffold large neuronal granules in the adult nervous system. Neuronal ELAV-like proteins directly bind mimi and mediate granule assembly, while Staufen maintains condensate integrity. mimi granules contain mRNAs and proteins involved in synaptic processes; granule loss in mimi mutant flies impairs nervous system maturity, neuropeptide-mediated signaling and causes phenotypes of neurodegeneration. Our work reports the first architectural RNA for a neuronal granule and provides a handle to interrogate functions of a condensate independently from those of its constituent proteins.
Project description:RNA-binding proteins and messenger RNAs assemble into ribonucleoprotein granules that regulate mRNA trafficking, local translation, and turnover. The dysregulation of RNA-protein condensation disturbs synaptic plasticity and neuron survival, and has been widely associated with human neurological disease. Neuronal granules are thought to condense around particular proteins that dictate the identity and composition of each granule type. Here, we show in Drosophila that a previously uncharacterized long non-coding RNA, mimi, is required to scaffold large neuronal granules in the adult nervous system. Neuronal ELAV-like proteins directly bind mimi and mediate granule assembly, while Staufen maintains condensate integrity. mimi granules contain mRNAs and proteins involved in synaptic processes; granule loss in mimi mutant flies impairs nervous system maturity, neuropeptide-mediated signaling and causes phenotypes of neurodegeneration. Our work reports the first architectural RNA for a neuronal granule and provides a handle to interrogate functions of a condensate independently from those of its constituent proteins.
Project description:RNA-binding proteins and messenger RNAs assemble into ribonucleoprotein granules that regulate mRNA trafficking, local translation, and turnover. The dysregulation of RNA-protein condensation disturbs synaptic plasticity and neuron survival, and has been widely associated with human neurological disease. Neuronal granules are thought to condense around particular proteins that dictate the identity and composition of each granule type. Here, we show in Drosophila that a previously uncharacterized long non-coding RNA, mimi, is required to scaffold large neuronal granules in the adult nervous system. Neuronal ELAV-like proteins directly bind mimi and mediate granule assembly, while Staufen maintains condensate integrity. mimi granules contain mRNAs and proteins involved in synaptic processes; granule loss in mimi mutant flies impairs nervous system maturity, neuropeptide-mediated signaling and causes phenotypes of neurodegeneration. Our work reports the first architectural RNA for a neuronal granule and provides a handle to interrogate functions of a condensate independently from those of its constituent proteins.
Project description:RNA-binding proteins and messenger RNAs assemble into ribonucleoprotein granules that regulate mRNA trafficking, local translation, and turnover. The dysregulation of RNA-protein condensation disturbs synaptic plasticity and neuron survival, and has been widely associated with human neurological disease. Neuronal granules are thought to condense around particular proteins that dictate the identity and composition of each granule type. Here, we show in Drosophila that a previously uncharacterized long non-coding RNA, mimi, is required to scaffold large neuronal granules in the adult nervous system. Neuronal ELAV-like proteins directly bind mimi and mediate granule assembly, while Staufen maintains condensate integrity. mimi granules contain mRNAs and proteins involved in synaptic processes; granule loss in mimi mutant flies impairs nervous system maturity, neuropeptide-mediated signaling and causes phenotypes of neurodegeneration. Our work reports the first architectural RNA for a neuronal granule and provides a handle to interrogate functions of a condensate independently from those of its constituent proteins.