PubMed · 1768208
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D K Oxley. 1991. Screening for hyperthyroidism.. https://pubmed.ncbi.nlm.nih.gov/1768208/
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Faithful chromosome segregation is fundamentally important for the maintenance of genome integrity and ploidy. By isolating conditional mutants defective in chromosome segregation in the fission yeast Schizosaccharomyces pombe, we identified a role for the essential gene pfs2 in chromosome dynamics. In the absence of functional Pfs2, chromosomal attachment to the mitotic spindle was defective, with consequent chromosome missegregation. Under these circumstances, multiple intracellular foci of spindle checkpoint proteins Bub1 and Mad2 were seen, and deletion of bub1 exacerbated the mitotic defects and the loss of cell viability that resulted from the loss of pfs2 function. Progression from G1 into S phase following release from nitrogen starvation also required pfs2+ function. The product of the orthologous Saccharomyces cerevisiae gene PFS2 is a component of a multiprotein complex required for 3'-end cleavage and polyadenylation of pre-mRNAs and, in keeping with the conservation of this essential function, an S. pombe pfs2 mutant was defective in mRNA 3'-end processing. Mutations in pfs2 were suppressed by overexpression of the putative mRNA 3'-end cleavage factor Cft1. These data suggest unexpected links between mRNA 3'-end processing and chromosome replication and segregation.
Acute promyelocytic leukaemia (APL) is characterised by a unique fusion transcript, PML/RAR alpha. We tested for this transcript in 35 APL patients who were in apparent remission after various treatments. 11 of 13 patients who tested positive 4 months after achieving remission were in relapse 1-4 months later. All 22 patients who tested negative at 4 months were disease-free after a further 3 months to five years. The test may therefore prove useful in determining the need for additional treatment during clinical remission.
The export of leukotriene (LT) C4 from human eosinophils, a carrier-mediated process that is temperature-dependent and saturable, was characterized further in eosinophils and in two human leukemia cell lines that do not present an intact 5-lipoxygenase pathway. In eosinophils, KG-1 cells, and dimethyl sulfoxide (DMSO)-differentiated HL-60 cells, the respective Q10 values for temperature-dependent LTC4 export were 3.7, 3.3, and 3.4 and for energy of activation were 28.2 kcal/mol, 23.0 kcal/mol, and 27.8 kcal/mol (1 kcal = 4.18 kJ). When human eosinophils, KG-1 cells, and DMSO-differentiated HL-60 cells were preloaded with defined amounts of intracellular LTC4 by incubation with LTA4 and with incremental amounts of a glutathione conjugate, S-dinitrophenyl glutathione (GS-DNP) by sequential incubation with 1-chloro-2,4-dinitrobenzene, GS-DNP inhibited the export of LTC4 in a dose-dependent manner. By plotting the ratio of total GS-DNP (cell retained plus released) to the sum of total GS-DNP plus total LTC4 against the percentage inhibition of LTC4 release, IC40 values of 0.839, 0.803, and 0.841 were obtained for eosinophils, KG-1 cells, and DMSO-differentiated HL-60 cells, respectively. When cells preloaded with LTC4 were resuspended in incremental concentrations of the organic acid transport inhibitor, probenecid, there was a dose-dependent decrease in LTC4 release; GS-DNP and probenecid inhibited LTC4 release in a cumulative fashion, whereas neither inhibited the release of LTB4 from preloaded nondifferentiated HL-60 cells. Therefore, LTC4 export from cells of bone marrow origin occurs through a probenecid-sensitive membrane carrier shared by other glutathione conjugates and distinct from the LTB4 carrier export system.