Biology subjects

Abid, K.

Publications and source records attributed to Abid, K..

3 recordsLinked to original sources

bioRxiv2022

Salicylic acid-related ribosomal protein CaSLP improves drought and Pst. DC3000 tolerance in pepper

The ribosomal protein SA plays an essential role in multiple aspects and is involved in plant growth and response to various stresses. Drought threatens pepper yield and quality. However, the resistance mechanism of pepper in response to drought are complex and not yet fully understood. Here, we describe the role of CaSLP in mediating pepper tolerance to drought stress. we found that CaSLP was highly expressed under drought and salicylic acid (SA) stress, and CaSLP was localized in cell nucleus and cytomembrane. Knockout of CaSLP gene significantly decreased the pepper drought tolerance, while transient expression of CaSLP leads to drought tolerance in pepper, and overexpression of the CaSLP dramatically increased the drought stress tolerance in Arabidopsis. Furthermore, exogenous spring salicylic acid enhanced drought tolerance. The characterization of resistance molecular mechanisms in the Pseudomonas syringae pv. Tomato DC3000 (Pst.DC3000) is of great significance for the pepper yield and quality, we found that CaSLP-knockdown pepper plants demonstrated decreased Pst.DC3000 tolerance, whereas ectopic expression of the CaSLP increased the Pst.DC3000 stress tolerance in Arabidopsis. Yeast two-hybrid (Y2H) and bimolecular fluorescence complementation (BiFC) results showed that CaNAC035 physically interacts with CaSLP in the cell nucleus, and the CaNAC035 was identified as an upstream partner of the CaPR1 promoter and activated the transcription. Taken together, our data demonstrated that CaSLP plays an essential role in the regulation of drought stress. Our study elucidates the roles of CaSLP response to drought stress tolerance. Furthermore, a possible regulatory model and molecular mechanisms under drought stress is proposed.

molecular biology↗

bioRxiv2021

eIF4E3 Forms an Active eIF4F Complex during Stresses (eIF4FS) Targeting mTOR and Re-Programs the Translatome.

The eIF4E are a family of initiation factors that bind the mRNA 5 cap, regulating the proteome and the cellular phenotype. eIF4E1 mediates global translation and its activity is controlled via the PI3K/AKT/mTOR pathway. mTOR down-regulation results in eIF4E1 sequestration into an inactive complex with the 4E binding proteins (4EBPs). The second member, eIF4E2, regulates the translatome during hypoxia. However, the exact function of the third member, eIF4E3, has remained elusive. We have dissected its function using a range of techniques. Starting from the observation that it does not interact with 4EBP1, we demonstrate that eIF4E3 recruitment into an eIF4F complex occurs when Torin1 inhibits the mTOR pathway. Ribo-seq studies demonstrate that this complex (eIF4FS) is translationally active only during stress and that it selects specific mRNA populations based on 5 TL (UTR) length. The interactome reveals that it associates with cellular proteins beyond the cognate initiation factors, suggesting that it may have "moon-lighting" functions. Finally, we provide evidence that cellular metabolism is altered in an eIF4E3 KO background but only upon Torin1 treatment. We propose that eIF4E3 acts as a second branch of the integrated stress response, re-programming the translatome to promote "stress resistance" and adaptation.

molecular biology↗

bioRxiv2020

Radiotherapy and chemotherapy alter migration of brain cancer cells before cell death

Although radiotherapy and most cancer drugs target the proliferation of cancer cells, it is metastasis, the complex process by which cancer cells spread from the primary tumor to other tissues and organs of the body where they form new tumors, that leads to over 90% of all cancer deaths. Thus, there is an urgent need for anti-metastasis strategies alongside chemotherapy and radiotherapy. An important step in the metastatic cascade is migration. It is the first step in metastasis via local invasion. Here we address the question whether ionizing radiation and/or chemotherapy might inadvertently promote metastasis and/or invasiveness by enhancing cell migration. We used a standard laboratory irradiator, Faxitron CellRad, to irradiate both non-cancer (HCN2 neurons) and cancer cells (T98G glioblastoma) with 2 Gy, 10 Gy and 20 Gy of X-rays. Paclitaxel (5 M) was used for chemotherapy. We then measured the attachment and migration of the cells using an electric cell substrate impedance sensing device. Both the irradiated HCN2 cells and T98G cells showed significantly (p < 0.01) enhanced migration compared to non-irradiated cells, within the first 20 to 40 hours following irradiation with 20 Gy. Our results suggest that cell migration should be a therapeutic target in anti-metastasis/anti-invasion strategies for improved radiotherapy and chemotherapy outcomes.

cancer biology↗