Project description:We found that L2HGDH mutants, in addition to accumulating L-2HG, are profoundly sensitive to hypoxic conditions (1% O2), in contrast to normal or heterozygote control flies which can survive and recover from hypoxia even after 12 hours of exposure. Here, we sought to investigate the trascriptomic changes associated with the response to hypoxia and recovery in both control and mutant backgrounds, with emphasis on the contrast between the normal and defective response at each time point.
Project description:ra09-03_sgs - mutants versus wt - Identification of new genes regulated by SGS1 and SGS6/UBP5 (two genes involved in PTGS) by analysis of the transcriptomes of sgs1 and sgs6 mutants compared to wild-type plants in the shoots of seedlings. The comparison between the transcriptomes of sgs3, chr11, chr17 simple mutants impaired differently in PTGS and development (juvenile-to-adult transition and bolting), and the transcriptomes of the sgs3 chr11, sgs3 chr17 double mutants showed additive effects on development (juvenile-to-adult transition and bolting), which allows a better understanding of the genetic link existing between SGS3 and its potential partners, CHR11 (which interacts with SGS3 in a two-hybrid assay and BiFC) and CHR17, 2 homologous proteins of the SWI/SNF2 family. Transcriptome comparison between mutants and wild-type plants L1 in the shoots of seedlings.
Project description:Identification of new genes regulated by RDR6 and SGS3 (two genes involved in PTGS) by analysis of the transcriptome of rdr6-1 and sgs3-1 mutants compared to wild-type plants in different tissues (flower and leaves). The comparison between transcriptome of rdr6-1 and sgs3-1 mutant alleles impaired in PTGS and development (juvenile-to-adult transition) and transcriptome of rdr6-5 and sgs3-3 alleles impaired only in PTGS would allowed identification of genes involved in the developmental default (zip phenotype) of the null alleles (rdr6-1 and sgs3-1 mutants).
Project description:ra09-03_sgs - mutants versus wt - Identification of new genes regulated by SGS1 and SGS6/UBP5 (two genes involved in PTGS) by analysis of the transcriptomes of sgs1 and sgs6 mutants compared to wild-type plants in the shoots of seedlings. The comparison between the transcriptomes of sgs3, chr11, chr17 simple mutants impaired differently in PTGS and development (juvenile-to-adult transition and bolting), and the transcriptomes of the sgs3 chr11, sgs3 chr17 double mutants showed additive effects on development (juvenile-to-adult transition and bolting), which allows a better understanding of the genetic link existing between SGS3 and its potential partners, CHR11 (which interacts with SGS3 in a two-hybrid assay and BiFC) and CHR17, 2 homologous proteins of the SWI/SNF2 family. Transcriptome comparison between mutants and wild-type plants L1 in the shoots of seedlings. 14 dye-swaps - gene knock-in (transgenic).
Project description:Identification of new genes regulated by RDR6 and SGS3 (two genes involved in PTGS) by analysis of the transcriptome of rdr6-1 and sgs3-1 mutants compared to wild-type plants in different tissues (flower and leaves). The comparison between transcriptome of rdr6-1 and sgs3-1 mutant alleles impaired in PTGS and development (juvenile-to-adult transition) and transcriptome of rdr6-5 and sgs3-3 alleles impaired only in PTGS would allowed identification of genes involved in the developmental default (zip phenotype) of the null alleles (rdr6-1 and sgs3-1 mutants). - Transcriptome of rdr6 and sgs3 mutants will be compared to the transcriptome of wild-type plants in flower and leaves. Further-more the comparison between transcriptome of rdr6-1 and sgs3-1 mutant alleles impaired in PTGS and development (juvenile-to-adult transition) and transcriptome of rdr6-5 and sgs3-3 alleles impaired only in PTGS will be done for flowers and leaves. Keywords: gene knock in (transgenic)
Project description:Skeletal muscle dysfunction in survivors of pneumonia is a major cause of lasting morbidity that disproportionately affects older individuals. We found that skeletal muscle recovery was impaired in aged compared with young mice after influenza A virus-induced pneumonia. In young mice, recovery of muscle loss was associated with expansion of tissue-resident skeletal muscle macrophages and downregulation of MHC II expression, followed by a proliferation of muscle satellite cells. These findings were absent in aged mice and in mice deficient in Cx3cr1. Transcriptomic profiling of tissue-resident skeletal muscle macrophages from aged compared with young mice showed downregulation of pathways associated with phagocytosis and proteostasis, and persistent upregulation of inflammatory pathways. Consistently, skeletal muscle macrophages from aged mice failed to downregulate MHCII expression during recovery from influenza A virus induced pneumonia and showed impaired phagocytic function in vitro. Like aged animals, mice deficient in the phagocytic receptor Mertk showed no macrophage expansion, MHCII downregulation or satellite cell proliferation and failed to recover skeletal muscle function after influenza A pneumonia. Our data suggest that a loss of phagocytic function in a CX3CR1+ tissue-resident skeletal muscle macrophage population in aged mice precludes satellite cell proliferation and recovery of skeletal muscle function after influenza A pneumonia.
Project description:The ability to rapidly respond to changes in temperature is critical for insects and other ectotherms living in variable environments. In a physiological process termed rapid cold-hardening (RCH), exposure to non-lethal low temperature allows many insects to significantly increase their cold tolerance in a matter of minutes to hours. Additionally, there are rapid changes in gene expression and cell physiology during recovery from cold injury, and we hypothesize that RCH may modulate some of these processes during recovery. In this study, we used a cDNA microarray to examine the molecular mechanisms of RCH and cold shock (CS) recovery in the flesh fly, Sarcophaga bullata. With our custom 2-color array, we measured expression of ~15,000 ESTs during RCH and during recovery from cold shock. Surprisingly, no transcripts were upregulated during RCH, and likewise, RCH had a minimal effect on the transcript signature during recovery from cold shock. However, during recovery from cold shock, we observed differential expression of ~1,400 ESTs, including a number of heat shock proteins, cytoskeletal components, and genes from several cell signaling pathways. Several gene pathways correlated well with metabolomics data, indicating that coordinated changes in gene expression and metabolism contribute to recovery from cold shock. Four treatment groups (C, RCH, CS+2R, RCH+CS+2R), four biological replicates of four pooled individuals for each treatment. Each phenotype was hybridized with the control, and the CS+2R and RCH+CS+2R groups were also hybridized together.