Multiple Regulatory Roles of a Novel Saccharomyces cerevisiae Protein, Encoded by YOL002c, in Lipid and Phosphate Metabolism

Karpichev, Igor V.; Cornivelli, Lizbeth; Small, Gillian M.

doi:10.1074/jbc.m202045200

Cited by 71 publications

(60 citation statements)

References 37 publications

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“…Therefore, it follows that alteration of membrane permeability by the IZH genes could play an important role in regulating tolerance to a membrane-active peptide like DsS3(1-16). In fact, this hypothesis is supported by the observation that deletion of IZH2 also confers resistance to the sterolbinding antibiotic nystatin which is known to interact with cell membranes (Karpichev et al, 2002).…”

Section: Discussionsupporting

confidence: 59%

“…Narasimhan et al (2005) discuss the pleiotrophic nature of IZH2 and IZH3 as a possible explanation for their mediation of osmotin tolerance. For example, the expression of both genes is induced by zinc deficiency and IZH2 is also induced by fatty acids (Karpichev et al, 2002). Thus, the IZH genes have been identified to play regulatory roles in lipid, phosphate and zinc metabolism.…”

Section: Discussionmentioning

confidence: 99%

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An amphibian‐derived, cationic, α‐helical antimicrobial peptide kills yeast by caspase‐independent but AIF‐dependent programmed cell death

Morton

Santos²,

Coote

2007

Molecular Microbiology

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SummaryThe dermaseptins are a family of antimicrobial peptides from the tree-frog Phyllomedusa sauvagii. Yeast exposed to dermaseptin S3(1-16), a truncated derivative of dermaseptin S3 with full activity, showed diagnostic markers of yeast apoptosis: the appearance of reactive oxygen species and fragmentation of nuclear DNA. This process was independent of the yeast caspase, Yca1p. Screening of a non-essential gene deletion collection in yeast identified genes that conferred resistance to dermaseptin S3(1-16): izh2D, izh3D, stm1D and aif1D, all known to be involved in regulating yeast apoptosis. The appearance of apoptotic markers was reduced in these strains when exposed to the peptide. Dermaseptin S3(1-16) was shown to interact with DNA, and cause DNA damage in vivo, a process known to trigger apoptosis. Supporting this, a dermaseptin S3(1-16) affinity column specifically purified Stm1p, Mre11p and Htb2p; DNAbinding proteins implicated in yeast apoptosis and DNA repair. Thus, amphibians may have evolved a mechanism to induce cell suicide in invading fungal pathogens.

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Section: Discussionsupporting

confidence: 59%

Section: Discussionmentioning

confidence: 99%

An amphibian‐derived, cationic, α‐helical antimicrobial peptide kills yeast by caspase‐independent but AIF‐dependent programmed cell death

Morton

Santos²,

Coote

2007

Molecular Microbiology

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“…In N. crassa most, if not all, blue light-regulated genes are subjected to photoadaptation, which depends on the presence of a functional VIVID protein (888)(889)(890). Similarly, ENV1 is a negative regulator of the BLR1/2 light input involved in photoadaptation; however, it does not functionally complement a vivid mutant (626,922). The T. atroviride ortholog of env1 is 60% identical and 75% similar to that of T. reesei.…”

Section: Photobiologymentioning

confidence: 99%

The Genomes of Three Uneven Siblings: Footprints of the Lifestyles of Three Trichoderma Species

Schmoll

Dattenböck

Carreras-Villaseñor

et al. 2016

Microbiol Mol Biol Rev

163

195

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SUMMARYThe genusTrichodermacontains fungi with high relevance for humans, with applications in enzyme production for plant cell wall degradation and use in biocontrol. Here, we provide a broad, comprehensive overview of the genomic content of these species for “hot topic” research aspects, including CAZymes, transport, transcription factors, and development, along with a detailed analysis and annotation of less-studied topics, such as signal transduction, genome integrity, chromatin, photobiology, or lipid, sulfur, and nitrogen metabolism inT. reesei,T. atroviride, andT. virens, and we open up new perspectives to those topics discussed previously. In total, we covered more than 2,000 of the predicted 9,000 to 11,000 genes of eachTrichodermaspecies discussed, which is >20% of the respective gene content. Additionally, we considered available transcriptome data for the annotated genes. Highlights of our analyses include overall carbohydrate cleavage preferences due to the different genomic contents and regulation of the respective genes. We found light regulation of many sulfur metabolic genes. Additionally, a new Golgi 1,2-mannosidase likely involved inN-linked glycosylation was detected, as were indications for the ability ofTrichodermaspp. to generate hybrid galactose-containingN-linked glycans. The genomic inventory of effector proteins revealed numerous compounds unique toTrichoderma, and these warrant further investigation. We found interesting expansions in theTrichodermagenus in several signaling pathways, such as G-protein-coupled receptors, RAS GTPases, and casein kinases. A particularly interesting feature absolutely unique toT. atrovirideis the duplication of the alternative sulfur amino acid synthesis pathway.

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“…This protein is structurally conserved from yeast to humans (especially in the 7 transmembrane domains). Interestingly, the yeast homologue (YOL002c) plays a key role in metabolic pathways that regulate lipid metabolism, such as fatty-acid oxidation (85). Since at that time there may have been 2 distinct adiponectin receptors, as was described above (67), we searched for a homologous gene in the human and mouse databases.…”

Section: Cloning Function and Regulation Of Adiponectin Receptorsmentioning

confidence: 99%

Adiponectin and adiponectin receptors in insulin resistance, diabetes, and the metabolic syndrome

Kadowaki¹

2006

Journal of Clinical Investigation

2,477

2,017

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Adiponectin is an adipokine that is specifically and abundantly expressed in adipose tissue and directly sensitizes the body to insulin. Hypoadiponectinemia, caused by interactions of genetic factors such as SNPs in the Adiponectin gene and environmental factors causing obesity, appears to play an important causal role in insulin resistance, type 2 diabetes, and the metabolic syndrome, which are linked to obesity. The adiponectin receptors, AdipoR1 and AdipoR2, which mediate the antidiabetic metabolic actions of adiponectin, have been cloned and are downregulated in obesity-linked insulin resistance. Upregulation of adiponectin is a partial cause of the insulin-sensitizing and antidiabetic actions of thiazolidinediones. Therefore, adiponectin and adiponectin receptors represent potential versatile therapeutic targets to combat obesity-linked diseases characterized by insulin resistance. This Review describes the pathophysiology of adiponectin and adiponectin receptors in insulin resistance, diabetes, and the metabolic syndrome.The prevalence of obesity has increased dramatically in recent years (1, 2). It is commonly associated with type 2 diabetes, coronary artery disease, and hypertension, and the coexistence of these diseases has been termed the metabolic syndrome (3-7). Insulin resistance is a key feature of these diseases and is defined as a state that requires more insulin to obtain the biological effects achieved by a lower amount of insulin in the normal state. Thus, any defects in the insulin signaling cascade can cause insulin resistance. Insulin stimulates a signaling network composed of a number of molecules, initiating the activation of insulin receptor tyrosine kinase and phosphorylation of the insulin receptor substrate (IRS) proteins (e.g., IRS-1 and IRS-2) (8). Among several components of the network, the signaling axis of IRS proteins and PI3K, which activates downstream serine/threonine kinases including Akt, regulates most of the metabolic actions of insulin, such as suppression of hepatic glucose production and activation of glucose transport in muscle and adipocytes (9). It is known that this pathway is impaired at the multiple steps through alterations in the protein levels and activities of the signaling molecules, enzymes, and transcription factors in insulin resistance caused by obesity, a state of increased adiposity (9).White adipose tissue (WAT) is a major site of energy storage and is important for energy homeostasis: it stores energy in the form of triglycerides during nutritional abundance and releases it as FFAs during nutritional deprivation (10, 11). While WAT provides a survival advantage in times of starvation, excess WAT is now linked to obesity-related health problems in the current nutritionally rich environment. Regulated by multiple hormonal signals, nuclear hormone receptors (12, 13), and the CNS (14), WAT has been increasingly recognized as an important endocrine organ that secretes a number of biologically active "adipokines" (15-19). Some of these adipokines have bee...

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Multiple Regulatory Roles of a Novel Saccharomyces cerevisiae Protein, Encoded by YOL002c, in Lipid and Phosphate Metabolism

Cited by 71 publications

References 37 publications

An amphibian‐derived, cationic, α‐helical antimicrobial peptide kills yeast by caspase‐independent but AIF‐dependent programmed cell death

An amphibian‐derived, cationic, α‐helical antimicrobial peptide kills yeast by caspase‐independent but AIF‐dependent programmed cell death

The Genomes of Three Uneven Siblings: Footprints of the Lifestyles of Three Trichoderma Species

Adiponectin and adiponectin receptors in insulin resistance, diabetes, and the metabolic syndrome

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