scholarly journals The dhp1+ gene, encoding a putative nuclear 5'->3' exoribonuclease, is required for proper chromosome segregation in fission yeast

2001 ◽  
Vol 29 (6) ◽  
pp. 1326-1333 ◽  
Author(s):  
T. Shobuike
2005 ◽  
Vol 15 (18) ◽  
pp. 1663-1669 ◽  
Author(s):  
Juraj Gregan ◽  
Peter K. Rabitsch ◽  
Benjamin Sakem ◽  
Ortansa Csutak ◽  
Vitaly Latypov ◽  
...  

2017 ◽  
Vol 28 (25) ◽  
pp. 3647-3659 ◽  
Author(s):  
Masashi Yukawa ◽  
Tomoki Kawakami ◽  
Masaki Okazaki ◽  
Kazunori Kume ◽  
Ngang Heok Tang ◽  
...  

Accurate chromosome segregation relies on the bipolar mitotic spindle. In many eukaryotes, spindle formation is driven by the plus-end–directed motor kinesin-5 that generates outward force to establish spindle bipolarity. Its inhibition leads to the emergence of monopolar spindles with mitotic arrest. Intriguingly, simultaneous inactivation of the minus-end–directed motor kinesin-14 restores spindle bipolarity in many systems. Here we show that in fission yeast, three independent pathways contribute to spindle bipolarity in the absence of kinesin-5/Cut7 and kinesin-14/Pkl1. One is kinesin-6/Klp9 that engages with spindle elongation once short bipolar spindles assemble. Klp9 also ensures the medial positioning of anaphase spindles to prevent unequal chromosome segregation. Another is the Alp7/TACC-Alp14/TOG microtubule polymerase complex. Temperature-sensitive alp7cut7pkl1 mutants are arrested with either monopolar or very short spindles. Forced targeting of Alp14 to the spindle pole body is sufficient to render alp7cut7pkl1 triply deleted cells viable and promote spindle assembly, indicating that Alp14-mediated microtubule polymerization from the nuclear face of the spindle pole body could generate outward force in place of Cut7 during early mitosis. The third pathway involves the Ase1/PRC1 microtubule cross-linker that stabilizes antiparallel microtubules. Our study, therefore, unveils multifaceted interplay among kinesin-dependent and -independent pathways leading to mitotic bipolar spindle assembly.


2018 ◽  
Vol 62 (11) ◽  
Author(s):  
Qiannan Liu ◽  
Fan Yao ◽  
Guanglie Jiang ◽  
Min Xu ◽  
Si Chen ◽  
...  

ABSTRACT The fight against resistance to antifungal drugs requires a better understanding of the underlying cellular mechanisms. In order to gain insight into the mechanisms leading to antifungal drug resistance, we performed a genetic screen on a model organism, Schizosaccharomyces pombe, to identify genes whose overexpression caused resistance to antifungal drugs, including clotrimazole and terbinafine. We identified the phb2+ gene, encoding a highly conserved mitochondrial protein, prohibitin (Phb2), as a novel determinant of reduced susceptibility to multiple antifungal drugs. Unexpectedly, deletion of the phb2+ gene also exhibited antifungal drug resistance. Overexpression of the phb2+ gene failed to cause drug resistance when the pap1+ gene, encoding an oxidative stress-responsive transcription factor, was deleted. Furthermore, pap1+ mRNA expression was significantly increased when the phb2+ gene was overexpressed or deleted. Importantly, either overexpression or deletion of the phb2+ gene stimulated the synthesis of NO and reactive oxygen species (ROS), as measured by the cell-permeant fluorescent NO probe DAF-FM DA (4-amino-5-methylamino-2′,7′-difluorofluorescein diacetate) and the ROS probe DCFH-DA (2′,7′-dichlorodihydrofluorescein diacetate), respectively. Taken together, these results suggest that Phb2 dysfunction results in reduced susceptibility to multiple antifungal drugs by increasing NO and ROS synthesis due to dysfunctional mitochondria, thereby activating the transcription factor Pap1 in fission yeast.


1992 ◽  
Vol 11 (13) ◽  
pp. 5111-5120 ◽  
Author(s):  
N.H. Waseem ◽  
K. Labib ◽  
P. Nurse ◽  
D.P. Lane

Chromosoma ◽  
2019 ◽  
Vol 128 (3) ◽  
pp. 385-396 ◽  
Author(s):  
Dmitriy Li ◽  
Marianne Roca ◽  
Raif Yuecel ◽  
Alexander Lorenz

2006 ◽  
Vol 5 (11) ◽  
pp. 1857-1865 ◽  
Author(s):  
Ji-Yoon Song ◽  
Joonseok Cha ◽  
Joon Lee ◽  
Jung-Hye Roe

ABSTRACT In the fission yeast Schizosaccharomyces pombe, the pgr1 + gene encoding glutathione (GSH) reductase (GR) is essentially required for cell survival. Depletion of GR caused proliferation arrest at the G1 phase of the cell cycle under aerobic conditions. Multicopy suppressors that restore growth were screened, and one effective suppressor was found to be the trx2 + gene, encoding a mitochondrial thioredoxin. This suggests that GR is critically required for some mitochondrial function(s). We found that GR resides in both cytosolic and organellar fractions of the cell. Depletion of GR lowered the respiration rate and the activity of oxidation-labile Fe-S enzymes such as mitochondrial aconitase and cytosolic sulfite reductase. Trx2 did not reverse the high ratio of oxidized glutathione to GSH or the low respiration rate observed in GR-depleted cells. However, it brought the activity of oxidation-labile Fe-S enzymes to a normal level, suggesting that the maintenance of Fe-S enzymes is a critical factor in the survival of S. pombe. The activity of succinate dehydrogenase, an oxidation-insensitive Fe-S enzyme, however, was not affected by GR depletion, suggesting that GR is not required for the biogenesis of the Fe-S cluster. The total iron content was greatly increased by GR depletion and was brought to a nearly normal level by Trx2. These results indicate that the essentiality of GR in the aerobic growth of S. pombe is derived from its role in maintaining oxidation-labile Fe-S enzymes and iron homeostasis.


2000 ◽  
Vol 28 (9) ◽  
pp. 2004-2011 ◽  
Author(s):  
E. J. Yoo ◽  
Y. H. Jin ◽  
Y. K. Jang ◽  
P. Bjerling ◽  
M. Tabish ◽  
...  

2014 ◽  
Vol 25 (24) ◽  
pp. 3900-3908 ◽  
Author(s):  
Judite Costa ◽  
Chuanhai Fu ◽  
V. Mohini Khare ◽  
Phong T. Tran

Proper chromosome segregation is of paramount importance for proper genetic inheritance. Defects in chromosome segregation can lead to aneuploidy, which is a hallmark of cancer cells. Eukaryotic chromosome segregation is accomplished by the bipolar spindle. Additional mechanisms, such as the spindle assembly checkpoint and centromere positioning, further help to ensure complete segregation fidelity. Here we present the fission yeast csi2+. csi2p localizes to the spindle poles, where it regulates mitotic microtubule dynamics, bipolar spindle formation, and subsequent chromosome segregation. csi2 deletion (csi2Δ) results in abnormally long mitotic microtubules, high rate of transient monopolar spindles, and subsequent high rate of chromosome segregation defects. Because csi2Δ has multiple phenotypes, it enables estimates of the relative contribution of the different mechanisms to the overall chromosome segregation process. Centromere positioning, microtubule dynamics, and bipolar spindle formation can all contribute to chromosome segregation. However, the major determinant of chromosome segregation defects in fission yeast may be microtubule dynamic defects.


2020 ◽  
Vol 52 (7) ◽  
pp. 702-707 ◽  
Author(s):  
Wenzhu Li ◽  
Xiangwei He

Abstract Canonical meiosis is characterized by two sequential rounds of nuclear divisions following one round of DNA replication—reductional segregation of homologous chromosomes during the first division and equational segregation of sister chromatids during the second division. Meiosis in an inverted order of two nuclear divisions—inverted meiosis has been observed in several species with holocentromeres as an adaptive strategy to overcome the obstacle in executing a canonical meiosis due to the holocentric chromosome structure. Recent findings of co-existence of inverted and canonical meiosis in two monocentric organisms, human and fission yeast, suggested that inverted meiosis could be common and also lead to the puzzle regarding the mechanistic feasibility for executing two meiosis programs simultaneously. Here, we discuss apparent conflicts for concurrent canonical meiosis and inverted meiosis. Furthermore, we attempt to provide a working model that may be compatible for both forms of meiosis.


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