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Titolo:
Correct regulation of the septation initiation network in Schizosaccharomyces pombe requires the activities of par1 and par2
Autore:
Jiang, W; Hallberg, RL;
Indirizzi:
Syracuse Univ, Dept Biol, Syracuse, NY 13244 USA Syracuse Univ Syracuse NY USA 13244 iv, Dept Biol, Syracuse, NY 13244 USA
Titolo Testata:
GENETICS
fascicolo: 4, volume: 158, anno: 2001,
pagine: 1413 - 1429
SICI:
0016-6731(200108)158:4<1413:CROTSI>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN PHOSPHATASE 2A; CELL-DIVISION CYCLE; MOLECULAR-GENETIC-ANALYSIS; SPINDLE-POLE BODIES; FISSION YEAST; SEPTUM FORMATION; CYTOKINESIS; KINASE; MITOSIS; ONSET;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Agriculture,Biology & Environmental Sciences
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Hallberg, RL Syracuse Univ, Dept Biol, 108 Coll Pl, Syracuse, NY 13244 USASyracuse Univ 108 Coll Pl Syracuse NY USA 13244 NY 13244 USA
Citazione:
W. Jiang e R.L. Hallberg, "Correct regulation of the septation initiation network in Schizosaccharomyces pombe requires the activities of par1 and par2", GENETICS, 158(4), 2001, pp. 1413-1429

Abstract

In Saccharomyces pombe, the initiation of cytokinesis is regulated by a septation initiation network (SIN). We previously reported that deletion of par1 and par2, two S. pombe genes encoding B ' regulatory subunits of protein phosphatase 2A, causes a multiseptation phenotype, very similar to that seen in hyperactive SIN mutants. In this study, we examined the genetic interactions between pai deletions and mutations in the genes encoding components of SIN and found that deletion of par1 and par2 suppressed the morphological and liability defects caused by overproduction of Byr4p and rescued a loss-of-function allele of spg1. However, par deletions could not suppress any mutations in genes downstream of spg1 in the SIN pathway. We showed further that, in suppressing the lethality of a spg1 loss-of-function allele, the correct localization of Cdc7p to the spindle pole body (SPB), which is normally lost in spg1 mutant cells, was restored. The fact that par mutant cells themselves exhibited a symmetric localization of Cdc7p to SPBs indicated a hyperactivity of SIN in such cells. On the basis of our epistasis analyses and cytological studies, we concluded that liar genes normally negatively regulate SIN at or upstream of cdc7, ensuring that multiple rounds of septation do not occur.

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Documento generato il 29/02/20 alle ore 15:11:27