Biology subjects

Zaidi, F.

Publications and source records attributed to Zaidi, F..

4 recordsLinked to original sources

bioRxiv2026

Assessing the impact of gamma irradiation on key biological traits of peach fruit fly, Bactrocera zonata (Diptera: Tephritidae) under laboratory conditions

Bactrocera zonata (Saunders) (Diptera: Tephritidae) poses a significant threat to global fruit production due to its high reproductive capacity and broad host range. This study aimed to evaluate the effects of gamma irradiation on key biological parameters of B. zonata. Six-day-old pupae were exposed to irradiation doses of 0, 30, 40, 50, 60, and 70 Gy, and subsequent developmental and reproductive traits were assessed to determine the impact of irradiation. Post-irradiation results revealed a dose-dependent trend. Higher doses ([≥]50 Gy) significantly reduced adult emergence, increased the incidence of partially emerged or deformed adults, and shortened adult longevity. Reproductive potential was significantly impaired in males irradiated at 60 and 70 Gy when mated with un-irradiated females, resulting in a marked decline in both fecundity and egg hatchability. Females irradiated at doses [≥]50 Gy failed to produce eggs when paired with either irradiated or non-irradiated males, indicating a high level of radio-sensitivity in female flies. Additionally, several traits in the F1 generation such as pupal recovery, pupal size, and adult development exhibited significant abnormalities and suggesting that the effects of irradiation may be transmitted to the next generation. Sterility was highest in males irradiated at 60 and 70 Gy, while females exhibited complete sterility at doses exceeding 40 Gy. The findings indicate that a dose of 70 Gy may be optimal for effective sterility induction in B. zonata. However, further detailed studies are required to standardize this dose, incorporating rigorous quality control measures to optimize its application in sterile insect technique (SIT) programs.

zoology↗

bioRxiv2024

Metastable condensates suppress conversion to amyloid fibrils

Stress granules form via co-condensation of RNA-binding proteins containing prion-like low complexity domains (PLCDs) with RNA molecules. Homotypic interactions among PLCDs can drive amyloid fibril formation that is enhanced by ALS-associated mutations. We report that condensation-versus fibril-driving homotypic interactions are separable for A1-LCD, the PLCD of hnRNPA1. Separable interactions lead to thermodynamically metastable condensates and globally stable fibrils. Interiors of condensates suppress fibril formation whereas interfaces have the opposite effect. ALS-associated mutations enhance the stability of fibrils and weaken condensate metastability, thus enhancing the rate of fibril formation. We designed mutations to enhance A1-LCD condensate metastability and discovered that stress granule disassembly in cells can be restored even when the designed variants carry ALS-causing mutations. Therefore, fibril formation can be suppressed by condensate interiors that function as sinks. Condensate sink potentials are influenced by their metastability, which is tunable through separable interactions even among minority components of stress granules.

biophysics↗

bioRxiv2022

High-Throughput Screening of the Saccharomyces cerevisiae Genome for 2-Amino-3-Methylimidazo Quinoline Resistance Identifies Colon Cancer-Associated Genes

Heterocyclic aromatic amines (HAAs) are potent carcinogenic agents found in charred meats and cigarette smoke. However, few eukaryotic resistance genes have been identified. We used Saccharomyces cerevisiae (budding yeast) to identify genes that confer resistance to 2-amino-3-methylimidazo[4,5-f]quinoline (IQ). CYP1A2 and NAT2 activate IQ to become a mutagenic nitrenium compound. We introduced an expression vector that contains human CYP1A2 and NAT2 genes into selected mutant strains and the diploid yeast deletion collection. The deletion libraries expressing CYP1A2 and NAT2 or no human genes were exposed to either 400 or 800 M IQ for five or ten generations. DNA barcodes were sequenced using the Illumina HiSeq 2500 platform and statistical significance was determined for exactly matched barcodes. Four screens for IQ resistance in the "humanized" collection identified 1160 unique ORFs, of which 337 were validated or duplicated in at least two screens. Two screens of the original yeast library identified 101 genes that overlap with the 337 previously identified. Selected genes were validated by growth curves, competitive growth assays, or trypan blue assays. Prominent among both sets are ribosomal protein genes, while nitrogen metabolism, cell wall synthesis, and phosphatase genes were identified among the "humanized" library. Protein complexes identified included the casein kinase 2 (CK2) and histone chaperone (HIR) complex. DNA repair genes included NTG1, RAD18, RAD9, PSY2 and UBC13. Polymorphisms in human NTHL1, the NTG1 ortholog, and RAD18 are risk factors for colon cancer. These studies thus provoke questions of whether genetic risk factors for colon cancer confer more HAA-associated toxicity.

genetics↗

bioRxiv2019

Patient-matched analysis identifies deregulated networks in prostate cancer to guide personalized therapeutic intervention

Prostate cancer (PrCa) is the second most common malignancy in men1. More than 50% of advanced prostate cancers display the TMPRSS2-ERG fusion2. Despite extensive cancer genome/transcriptome2-4 and phosphoproteome5 data, little is known about the impact of mutations and altered transcription on regulatory networks in the PrCa of individual patients. Using patient-matched normal and tumor samples, we established somatic variations and differential transcriptome profiles of primary ERG-positive prostate cancers. Integration of protein-protein interaction and gene-regulatory network databases6, 7 defined highly diverse patient-specific network alterations. We found that different components of a given regulatory pathway were altered by novel and known mutations and/or aberrant gene expression, including deregulated ERG targets, such that different sets of pathways were altered in each individual PrCa. In a given PrCa, several deregulated pathways share common factors, predicting synergistic effects on cancer progression. Our integrated analysis provides a paradigm to identify key deregulated factors within regulatory networks to guide personalized therapies.

genomics↗