High impact information on SUT1

• In contrast to SUT1, SUT4 is expressed predominantly in minor veins in source leaves, where high-capacity sucrose transport is needed for phloem loading [1].
• In potato and tomato, SUT4 was immunolocalized specifically to enucleate sieve elements, indicating that like SUT1, macromolecular trafficking is required to transport the mRNA or the protein from companion cells through plasmodesmata into the sieve elements [1].
• Examination of the subcellular distribution of sterols in these uptake mutants by cell fractionation and fluorescence microscopy indicates that some of the mutants block incorporation of cholesterol into the plasma membrane, a presumably early step in sterol uptake [2].
• These results indicate that a hitherto uncharacterized mitochondrial function is required for sterol uptake and/or transport under anaerobic conditions and are discussed in light of the fact that mitochondrial import of cholesterol is required for steroidogenesis in vertebrate cells [2].
• Ketoconazole exposure primarily affected genes involved in ergosterol biosynthesis and sterol uptake; caspofungin exposure affected genes involved in cell wall integrity; and 5-FC affected genes involved in DNA and protein synthesis, DNA damage repair, and cell cycle control [3].

Biological context of SUT1

• Upon SUT1 constitutive expression in aerobiosis, the repression is released, allowing enhanced transcription of the reporter gene [4].
• A higher SUT1 gene dosage leads to a modest, but significant, increase in sterol uptake under aerobic conditions [5].
• SUT1 constitutive expression in aerobiosis suppressed the ts phenotype of the sec14-1 mutation, restored growth of the sec14-null mutant and corrected the translocation defect of the vacuolar carboxypeptidase Y [6].
• SUT1 suppresses sec14-1 through upregulation of CSR1 in Saccharomyces cerevisiae [6].
• A total of 121 ORFs (open reading frames) were significantly and differentially expressed after SUT1 overexpression, 61 down-regulated and 60 up-regulated [7].

Anatomical context of SUT1

• In contrast to lipoprotein-mediated sterol uptake, free sterol influx by eukaryotic cells is poorly understood [8].

Associations of SUT1 with chemical compounds

• Unexpectedly, SUT1 constitutive expression led to a parallel significant increase in endogenous sterol biosynthesis [5].
• In P. stipitis, transcription of SUT1 was strongly induced by glucose and was independent of the oxygen supply [9].
• Similar to the sucrose transporter SUT1, StAAP1 expression was induced during the sink-to-source transition, indicating a role in phloem loading [10].
• Sodium azide and vanadate inhibited sterol uptake, consistent with the participation of ATP-binding cassette transporters [8].
• Regulation of ergosterol biosynthesis and sterol uptake in a sterol-auxotrophic yeast [11].

Physical interactions of SUT1

• Furthermore, the N-terminal half of the low-affinity SUT2 interacts functionally with the C-terminal half of SUT1 [12].

Other interactions of SUT1

• Within the promoter sequence of one of these genes, DAN1, we identified the region responsive to SUT1 and showed that it has a strong repressive activity when cloned in the vicinity of distinct promoters [4].
• Moreover, here we present new data showing that the structurally related YPR009 gene (SUT2) is a functional homologue of SUT1, and that both gene products may represent two novel yeast regulatory proteins involved in sterol uptake [5].
• We provide evidence that the repression is promoted by the Cyc8p(Ssn6p)-Tup1p co-repressor and that release of repression is the result of a physical interaction between Sut1p and Cyc8p [4].
• We replaced the SUT1 promoter with the constitutive PMA1 gene promoter in order to enhance its transcription [5].
• In addition, SUT1 effects on both sec14-1 suppression and on free sterol composition were abolished in a csr1-null background, showing that this gene acts downstream of SUT1 [6].

Analytical, diagnostic and therapeutic context of SUT1

• A genome-wide approach using DNA microarray was used to identify the mediators of SUT1 effects on aerobic sterol uptake [7].
• Northern blot analysis revealed that SUT1 is a new member of the hypoxic gene family [13].
• The upc2-1 point mutation responsible for aerobic sterol uptake was duplicated in the homologous carboxy region of the YLR228c ORF using site-directed mutagenesis [14].

References