ArticleThe Journal of nutrition2007
Susceptibility to heat stress and aberrant gene expression patterns in holocarboxylase synthetase-deficient Drosophila melanogaster are caused by decreased biotinylation of histones, not of carboxylases.
Article in The Journal of nutrition, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 42 citations in OpenAlex.
- Reduction of oocyte lipid droplets and meiotic failure due to biotin deficiency was not rescued by restoring the biotin nutritional status.Nutrition research and practice · 2022Article
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- Article
- Sex Differences in Intestinal Carbohydrate Metabolism Promote Food Intake and Sperm Maturation.Cell · 2019Article
- Holocarboxylase synthetase interacts physically with nuclear receptor co-repressor, histone deacetylase 1 and a novel splicing variant of histone deacetylase 1 to repress repeats.The Biochemical journal · 2014Article
- Antioxidant status of serum, muscle, intestine and hepatopancreas for fish fed graded levels of biotin.Fish physiology and biochemistry · 2014Article
- Article
- Biotinylation of lysine 16 in histone H4 contributes toward nucleosome condensation.Archives of biochemistry and biophysics · 2013Article
- K16-biotinylated histone H4 is overrepresented in repeat regions and participates in the repression of transcriptionally competent genes in human Jurkat lymphoid cells.The Journal of nutritional biochemistry · 2012Article
- Novel histone biotinylation marks are enriched in repeat regions and participate in repression of transcriptionally competent genes.The Journal of nutritional biochemistry · 2011Article
- Biotin regulates the expression of holocarboxylase synthetase in the miR-539 pathway in HEK-293 cells.The Journal of nutrition · 2010Article
- K12-biotinylated histone H4 is enriched in telomeric repeats from human lung IMR-90 fibroblasts.The Journal of nutritional biochemistry · 2010Article
- The polypeptide Syn67 interacts physically with human holocarboxylase synthetase, but is not a target for biotinylation.Archives of biochemistry and biophysics · 2010Article
- Repression of transposable elements by histone biotinylation.The Journal of nutrition · 2009Article
- Gamma-ray up-regulated holocarboxylase synthetase gene.Cellular and molecular neurobiology · 2009Article
- N- and C-terminal domains in human holocarboxylase synthetase participate in substrate recognition.Molecular genetics and metabolism · 2009Article
- Nitric oxide signaling depends on biotin in Jurkat human lymphoma cells.The Journal of nutrition · 2009Article
- Biotinyl-methyl 4-(amidomethyl)benzoate is a competitive inhibitor of human biotinidase.The Journal of nutritional biochemistry · 2008Article
- Biotin and biotinidase deficiency.Expert review of endocrinology & metabolism · 2008Article
- Epigenetic regulation of chromatin structure and gene function by biotin: are biotin requirements being met?Nutrition reviews · 2008Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Previously, we discovered that holocarboxylase synthetase (HCS) is a chromatin-associated protein in Drosophila melanogaster and that HCS deficiency alters chromatin structure and gene expression patterns, leading to decreased heat tolerance. The effects of HCS deficiency were attributed to decreased biotinylation of histones. However, HCS is known to mediate biotinylation of carboxylases in cytoplasm and mitochondria in addition to mediating biotinylation of histones. A challenge posed by the genetic analysis of HCS is to distinguish between the effects of decreased biotinylation of carboxylases from the effects of decreased histone biotinylation in the gene expression patterns and phenotypes observed in HCS-deficient flies. Here, we tested whether 3-methylcrotonyl-CoA carboxylase (MCC) mutant flies exhibit gene expression patterns and heat susceptibility similar to that in HCS-deficient Drosophila. Biotin transporter [sodium-dependent multivitamin transporter (SMVT)] mutants were used to investigate effects of cellular biotin depletion on gene expression and heat susceptibility. Deficiencies of MCC and SMVT in mutant flies were confirmed by real-time PCR, streptavidin blotting of holocarboxylases, and analysis of MCC activities; expression of HCS and biotinylation of histones were not altered in MCC and SMVT mutants. Gene expression patterns in MCC and SMVT mutants were different from that seen with HCS-deficient flies, as judged by the abundance of mRNA coding for defective chorion 1, chitin-binding peritrophin-A, dopamine receptor 2, and yolk protein 2. MCC mutants exhibited increased resistance to heat stress compared with wild-type flies. We conclude that gene expression patterns and phenotypes in HCS-deficient flies in previous studies are caused by decreased biotinylation of histones rather than MCC.
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