daf-2 mutant vs N2 (Zarse 2012)

Impaired Insulin-/IGF1-Signaling Extends Life Span by Promoting Mitochondrial L-Proline Catabolism to Induce a Transient ROS-Signal

Top level analysis object for all of the S. ratti RNASeq analyses.

Following the subprojects to find all S. ratti RNASeq analyses.

C. elegans gene expression in response to Salmonella enterica infection and recovery by Tetracycline treatment

(Part 1) Gene expression profiles of C. elegans in response to a 120 hour S. enterica infection. Synchronized larval stage 1 (L1) animals were exposed to S. enterica SL1344 for 36, 72, 96, or 120 hours. As an uninfected control, synchronized L1 animals were exposed to E. coli OP50 for 36 hours. (Part 2) Gene expression profiles of C. elegans in response to Tetracycline-mediated recovery from 72 hour and 96 hour S. enterica infections. Synchronized L1 animals were exposed to S. enterica SL1344 for 72 hours and then shifted to E. coli HT115 plus Tetracycline plates for 24 hours to resolve the infection. Synchronized L1 animals were exposed to S. enterica SL1344 for 96 hours and then shifted to E. coli HT115 plus Tetracycline plates for 24 hours to resolve the infection.

PQM-1 controls hypoxic survival via regulation of lipid metabolism.

Worms were exposed to 5 mM CoCl2 at the early day 1 of adulthood stage for 6 hr and 20 hr. Untreated worms were used as controls. Worms were collected, RNA isolated and hybridized on 4x44K C. elegans arrays (Agilent) at 60C overnight, as previously described 1). Three biological replicates were used. Significant differentially-expressed gene sets were identified using one or two-class SAM 2). 1) Shaw, W. M., Luo, S., Landis, J., Ashraf, J. & Murphy, C. T. The C. elegans TGF-beta Dauer pathway regulates longevity via insulin signaling. Curr Biol 17, 1635-1645, doi:10.1016/j.cub.2007.08.058 (2007). 2) Tusher, V. G., Tibshirani, R. & Chu, G. Significance analysis of microarrays applied to the ionizing radiation response. Proc Natl Acad Sci U S A 98, 5116-5121, doi:10.1073/pnas.091062498 (2001).

Mitochondrial proteomic profiles of N2 and daf-2(e1370)

Reproductive aging is one of the earliest human aging phenotypes, and mitochondrial dysfunction has been linked to a decline in oocyte quality. However, it is not known which mitochondrial metabolic processes are critical for oocyte quality maintenance with age. To understand how mitochondrial processes contribute to C. elegans oocyte quality, authors characterized the mitochondrial proteomes of young and aged wild-type and long-reproductive daf-2 mutants. The mitochondrial proteomic profiles of young wild-type and daf-2 worms are similar and share upregulation of branched-chain amino acid (BCAA) metabolism pathway enzymes. Reduction of bcat-1 shortens reproduction, elevates mitochondrial ROS levels, and shifts mitochondrial localization. Moreover, bcat-1 knockdown decreases daf-2s oocyte quality and reduces reproductive capability, indicating the importance of this pathway in the maintenance of oocyte quality with age. Importantly, we can delay oocyte quality deterioration and extend reproduction in wild-type animals both by bcat-1 overexpression and by supplementing with Vitamin B1, a cofactor needed for BCAA metabolism.

Mitochondrial proteomic profiles of N2 and daf-2(e1370)

Reproductive aging is one of the earliest human aging phenotypes, and mitochondrial dysfunction has been linked to a decline in oocyte quality. However, it is not known which mitochondrial metabolic processes are critical for oocyte quality maintenance with age. To understand how mitochondrial processes contribute to C. elegans oocyte quality, authors characterized the mitochondrial proteomes of young and aged wild-type and long-reproductive daf-2 mutants. The mitochondrial proteomic profiles of young wild-type and daf-2 worms are similar and share upregulation of branched-chain amino acid (BCAA) metabolism pathway enzymes. Reduction of bcat-1 shortens reproduction, elevates mitochondrial ROS levels, and shifts mitochondrial localization. Moreover, bcat-1 knockdown decreases daf-2s oocyte quality and reduces reproductive capability, indicating the importance of this pathway in the maintenance of oocyte quality with age. Importantly, we can delay oocyte quality deterioration and extend reproduction in wild-type animals both by bcat-1 overexpression and by supplementing with Vitamin B1, a cofactor needed for BCAA metabolism.

Mitochondrial proteomic profiles of N2 and daf-2(e1370)

Reproductive aging is one of the earliest human aging phenotypes, and mitochondrial dysfunction has been linked to a decline in oocyte quality. However, it is not known which mitochondrial metabolic processes are critical for oocyte quality maintenance with age. To understand how mitochondrial processes contribute to C. elegans oocyte quality, authors characterized the mitochondrial proteomes of young and aged wild-type and long-reproductive daf-2 mutants. The mitochondrial proteomic profiles of young wild-type and daf-2 worms are similar and share upregulation of branched-chain amino acid (BCAA) metabolism pathway enzymes. Reduction of bcat-1 shortens reproduction, elevates mitochondrial ROS levels, and shifts mitochondrial localization. Moreover, bcat-1 knockdown decreases daf-2s oocyte quality and reduces reproductive capability, indicating the importance of this pathway in the maintenance of oocyte quality with age. Importantly, we can delay oocyte quality deterioration and extend reproduction in wild-type animals both by bcat-1 overexpression and by supplementing with Vitamin B1, a cofactor needed for BCAA metabolism.

Mitochondrial proteomic profiles of N2 and daf-2(e1370)

Reproductive aging is one of the earliest human aging phenotypes, and mitochondrial dysfunction has been linked to a decline in oocyte quality. However, it is not known which mitochondrial metabolic processes are critical for oocyte quality maintenance with age. To understand how mitochondrial processes contribute to C. elegans oocyte quality, authors characterized the mitochondrial proteomes of young and aged wild-type and long-reproductive daf-2 mutants. The mitochondrial proteomic profiles of young wild-type and daf-2 worms are similar and share upregulation of branched-chain amino acid (BCAA) metabolism pathway enzymes. Reduction of bcat-1 shortens reproduction, elevates mitochondrial ROS levels, and shifts mitochondrial localization. Moreover, bcat-1 knockdown decreases daf-2s oocyte quality and reduces reproductive capability, indicating the importance of this pathway in the maintenance of oocyte quality with age. Importantly, we can delay oocyte quality deterioration and extend reproduction in wild-type animals both by bcat-1 overexpression and by supplementing with Vitamin B1, a cofactor needed for BCAA metabolism.

Mitochondrial proteomic profiles of N2 and daf-2(e1370)

Reproductive aging is one of the earliest human aging phenotypes, and mitochondrial dysfunction has been linked to a decline in oocyte quality. However, it is not known which mitochondrial metabolic processes are critical for oocyte quality maintenance with age. To understand how mitochondrial processes contribute to C. elegans oocyte quality, authors characterized the mitochondrial proteomes of young and aged wild-type and long-reproductive daf-2 mutants. The mitochondrial proteomic profiles of young wild-type and daf-2 worms are similar and share upregulation of branched-chain amino acid (BCAA) metabolism pathway enzymes. Reduction of bcat-1 shortens reproduction, elevates mitochondrial ROS levels, and shifts mitochondrial localization. Moreover, bcat-1 knockdown decreases daf-2s oocyte quality and reduces reproductive capability, indicating the importance of this pathway in the maintenance of oocyte quality with age. Importantly, we can delay oocyte quality deterioration and extend reproduction in wild-type animals both by bcat-1 overexpression and by supplementing with Vitamin B1, a cofactor needed for BCAA metabolism.

Conserved nutrient sensor O-GlcNAc transferase is integral to the C. elegans pathogen-specific immune response

Discriminating pathogenic bacteria from energy-harvesting commensals is key to host immunity. Using mutants defective in the enzymes of O-linked N-acetylglucosamine (O-GlcNAc) cycling, we examined the role of this nutrient-sensing pathway in the Caenorhabidits elegans innate immune response. Using whole genome transcriptional profiling, O-GlcNAc cycling mutants exhibited deregulation of unique stress- and immune-responsive genes as well as genes shared with the p38 MAPK/PMK-1 pathway. Moreover, genetic analysis showed that deletion of O-GlcNAc transferase (ogt-1) yielded animals hypersensitive to the human pathogen S. aureus but not to P. aeruginosa. Genetic interaction studies further revealed that nutrient-responsive OGT-1 acts through the conserved -catenin (BAR-1) pathway and in concert with p38 MAPK/PMK-1 to modulate the immune response to S. aureus. The participation of the nutrient sensor O-GlcNAc transferase in an immunity module conserved from C. elegans to humans reveals an unexplored nexus between nutrient availability and a pathogen-specific immune response.