Genetic Interaction between Ribosome Biogenesis and Inositol Polyphosphate Metabolism inSaccharomyces cerevisiae

2009 ◽  
Vol 73 (2) ◽  
pp. 443-446 ◽  
Author(s):  
Chihiro HORIGOME ◽  
Ryo IKEDA ◽  
Takafumi OKADA ◽  
Kazuhiko TAKENAMI ◽  
Keiko MIZUTA
Keyword(s):  
Ribosome Biogenesis ◽  
Genetic Interaction ◽  
Inositol Polyphosphate ◽  
Polyphosphate Metabolism

Myo-inositol Polyphosphate Metabolism and Signaling in Arabidopsis

2013 ◽  
Vol 48 (1) ◽  
pp. 94-106
Author(s):  
Wu Li ◽  
Wang Ruozhong ◽  
Xu Wenzhong
Keyword(s):  
Inositol Polyphosphate ◽  
Polyphosphate Metabolism

scholarly journals Genetic Interaction Screens with Ordered Overexpression and Deletion Clone Sets Implicate the Escherichia coli GTPase YjeQ in Late Ribosome Biogenesis

2008 ◽  
Vol 190 (7) ◽  
pp. 2537-2545 ◽  
Author(s):  
Tracey L. Campbell ◽  
Eric D. Brown
Keyword(s):  
Escherichia Coli ◽  
Ribosome Biogenesis ◽  
Slow Growth ◽  
Genetic Interaction ◽  
Initiation Factor ◽  
Genetic Screens ◽  
Genomic Libraries ◽  
Initiation Factor 2 ◽  
Bona Fide

ABSTRACT The Escherichia coli protein YjeQ is a circularly permuted GTPase that is broadly conserved in bacteria. An emerging body of evidence, including cofractionation and in vitro binding to the ribosome, altered polysome profiles after YjeQ depletion, and stimulation of GTPase activity by ribosomes, suggests that YjeQ is involved in ribosome function. The growth of strains lacking YjeQ in culture is severely compromised. Here, we probed the cellular function of YjeQ with genetic screens of ordered E. coli genomic libraries for suppressors and enhancers of the slow-growth phenotype of a ΔyjeQ strain. Screening for suppressors using an ordered library of 374 clones overexpressing essential genes and genes associated with ribosome function revealed that two GTPases, Era and initiation factor 2, ameliorated the growth and polysome defects of the ΔyjeQ strain. In addition, seven bona fide enhancers of slow growth were identified (Δtgt, ΔksgA, ΔssrA, ΔrimM, ΔrluD, ΔtrmE/mnmE, and ΔtrmU/mnmA) among 39 deletions (in genes associated with ribosome function) that we constructed in the ΔyjeQ genetic background. Taken in context, our work is most consistent with the hypothesis that YjeQ has a role in late 30S subunit biogenesis.

Kinetic Analysis of Novel Inhibitors of Inositol Polyphosphate Metabolism

1994 ◽  
Vol 200 (1) ◽  
pp. 8-15 ◽  
Author(s):  
P.M. Hansbro ◽  
P.S. Foster ◽  
C.S. Liu ◽  
B.V.L. Potter ◽  
M.A. Denborough
Keyword(s):  
Kinetic Analysis ◽  
Inositol Polyphosphate ◽  
Polyphosphate Metabolism

scholarly journals Multiple isomers of inositol pentakisphosphate in Epstein-Barr-virus- transformed (T5-1) B-lymphocytes. Identification of inositol 1,3,4,5,6-pentakisphosphate, d-inositol 1,2,4,5,6-pentakisphosphate and l-inositol 1,2,4,5,6-pentakisphosphate

1991 ◽  
Vol 280 (2) ◽  
pp. 323-329 ◽  
Author(s):  
F M McConnell ◽  
L R Stephens ◽  
S B Shears
Keyword(s):  
Inositol Polyphosphate ◽  
Permeabilized Cells ◽  
Barr Virus ◽  
Epstein Barr ◽  
Polyphosphate Metabolism ◽  
And Function ◽  
Lymphocyte Cell ◽  
Lymphocyte Cell Line

Substantial amounts of three [3H]InsP5 isomers were detected in [3H]inositol-labelled human lymphoblastoid (T5-1) cells. Their structures were determined by h.p.l.c. [Phillippy & Bland (1988) Anal. Biochem. 175, 162-166], and by utilizing a stereospecific D-inositol 1,2,4,5,6-pentakisphosphate 3-kinase from Dictyostelium discoideum [Stephens & Irvine (1990) Nature (London) 346, 580-583]. The structures were: inositol 1,3,4,5,6-pentakisphosphate, D-inositol 1,2,4,5,6-pentakisphosphate and L-inositol 1,2,4,5,6-pentakisphosphate. The relative proportions of these isomers (approx. 73:14:14 respectively) were unaffected by cross-linking anti-IgD receptors. The T5-1 cells also contained InsP6 and three Ins P4s, which were identified as the 1,3,4,5, 1,3,4,6 and 3,4,5,6 isomers. In incubations with permeabilized T5-1 cells, both 1,3,4,6 and 3,4,5,6 isomers of InsP4 were phosphorylated solely to Ins(1,3,4,5,6)P5. Permeabilized cells also dephosphorylated InsP6, even in the presence of a large excess of glucose 6-phosphate to saturate non-specific phosphatases. In the latter experiments the following isomers of InsP5 accumulated: D- and/or L-Ins(1,2,3,4,5)P5, plus D- and/or L-Ins(1,2,4,5,6)P5. This demonstration that multiple isomers of InsP5 may be formed in vivo and in vitro by a transformed lymphocyte cell line adds a new level of complexity to the study of inositol polyphosphate metabolism and function.

scholarly journals MINPP1 prevents intracellular accumulation of the cation chelator inositol hexakisphosphate and is mutated in Pontocerebellar Hypoplasia

2020 ◽  
Author(s):  
Ekin Ucuncu ◽  
Karthyayani Rajamani ◽  
Miranda S.C. Wilson ◽  
Daniel Medina-Cano ◽  
Nami Altin ◽  
...  
Keyword(s):  
Critical Role ◽  
Distinct Type ◽  
Cell Physiology ◽  
Inositol Polyphosphate ◽  
Loss Of Function ◽  
Pontocerebellar Hypoplasia ◽  
Inositol Polyphosphates ◽  
Induced Pluripotent ◽  
Basal Ganglia Involvement ◽  
Polyphosphate Metabolism

ABSTRACTInositol polyphosphates are vital metabolic and secondary messengers, involved in diverse cellular functions. Therefore, tight regulation of inositol polyphosphate metabolism is essential for proper cell physiology. Here, we describe an early-onset neurodegenerative syndrome caused by loss-of-function mutations in the multiple inositol polyphosphate phosphatase 1 gene (MINPP1). Patients were found to have a distinct type of Pontocerebellar Hypoplasia with typical basal ganglia involvement on neuroimaging. We found that patient-derived and genome edited MINPP1-/- induced pluripotent stem cells (iPSCs) are not able to differentiate efficiently into neurons. MINPP1 deficiency results in an intracellular imbalance of the inositol polyphosphate metabolism. This metabolic defect is characterized by an accumulation of highly phosphorylated inositols, mostly inositol hexakiphosphate (IP6), detected in HEK293, fibroblasts, iPSCs and differentiating neurons lacking MINPP1. In mutant cells, higher IP6 level is expected to be associated with an increased chelation of intracellular cations, such as iron or calcium, resulting in decreased levels of available ions. These data suggest the involvement of IP6-mediated chelation on Pontocerebellar Hypoplasia disease pathology and thereby highlight the critical role of MINPP1 in the regulation of human brain development and homeostasis.

scholarly journals Investigation of RNA metabolism through large-scale genetic interaction profiling in yeast

2020 ◽  
Author(s):  
Laurence Decourty ◽  
Christophe Malabat ◽  
Emmanuel Frachon ◽  
Alain Jacquier ◽  
Cosmin Saveanu
Keyword(s):  
Large Scale ◽  
Gene Deletion ◽  
Genetic Interaction ◽  
Mrna Translation ◽  
Rna Metabolism ◽  
Inositol Polyphosphate ◽  
Growth Defects ◽  
Gene Expression Alteration ◽  
Analysis Strategy ◽  
Mrna Destabilization

AbstractGene deletion and gene expression alteration can lead to growth defects that are amplified or reduced when a second mutation is present in the same cells. We performed 154 genetic interaction mapping (GIM) screens with mutants related with RNA metabolism and measured growth rates of about 700 000 Saccharomyces cerevisiae double mutant strains. The screens used the gene deletion collection in addition to a set of 900 strains in which essential genes were affected by mRNA destabilization (DAmP). To analyze the results we developed RECAP, a strategy that validates genetic interaction profiles by comparison with gene co-citation frequency, and identified links between 1 471 genes and 117 biological processes. To validate specific results, we tested and confirmed a link between an inositol polyphosphate hydrolase complex and mRNA translation initiation. Altogether, the results and the newly developed analysis strategy should represent a useful resource for discovery of gene function in yeast.

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