G1-Cyclin2 (Cln2) promotes chromosome hypercondensation in eco1/ctf7 rad61 null cells during hyperthermic stress in Saccharomyces cerevisiae.
G1-Cyclin2 (Cln2) promotes chromosome hypercondensation in eco1/ctf7 rad61 null cells during hyperthermic stress in Saccharomyces cerevisiae.
复制标题
DOI：
10.1093/g3journal/jkac157
复制
发表时间：
2022-07-29
影响因子：
2.6
通讯作者：
Skibbens, Robert, V
中科院分区：
文献类型：
--
作者：
Buskirk, Sean;Skibbens, Robert, V
关键词：
Eco1/Ctf7 是一种高度保守的乙酰转移酶，可激活粘连蛋白复合物，对姐妹染色单体凝聚、染色体浓缩、DNA 损伤修复、核仁完整性和基因转录至关重要。 ECO1 的人类同源物 (ESCO2/EFO2) 或编码粘连蛋白亚基的基因突变，会导致严重的发育异常和智力障碍，分别称为罗伯茨综合征和科妮莉亚德兰格综合征。在酵母中，ECO1 的缺失会导致细胞死亡。然而，RAD61（人类中的 WAPL）的共缺失会产生活的酵母细胞。然而，这些eco1 rad61双突变体表现出严重的温度敏感生长缺陷，表明Eco1或粘连蛋白通过独立于Rad61发生的机制对高温应激作出反应。在这里，我们报告G1细胞周期蛋白CLN2的缺失挽救了eco1 rad61突变细胞原本表现出的温度敏感性致死性，使得三重突变细胞在较宽的温度范围内表现出强劲的生长。虽然 Cln1、Cln2 和 Cln3 是功能冗余的 G1 细胞周期蛋白，但 CLN1 和 CLN3 缺失都无法挽救 eco1 rad61 双突变体表现出的温度敏感生长缺陷。我们进一步提供证据表明，CLN2 缺失可挽救独立于 START 的高温生长缺陷，并影响染色体凝缩状态。这些发现揭示了 Cln2 的新作用，在 G1 细胞周期蛋白家族中是独一无二的，并且对于高温应激期间的粘连蛋白调节至关重要。
Eco1/Ctf7 is a highly conserved acetyltransferase that activates cohesin complexes and is critical for sister chromatid cohesion, chromosome condensation, DNA damage repair, nucleolar integrity, and gene transcription. Mutations in the human homolog of ECO1 (ESCO2/EFO2), or in genes that encode cohesin subunits, result in severe developmental abnormalities and intellectual disabilities referred to as Roberts syndrome and Cornelia de Lange syndrome, respectively. In yeast, deletion of ECO1 results in cell inviability. Codeletion of RAD61 (WAPL in humans), however, produces viable yeast cells. These eco1 rad61 double mutants, however, exhibit a severe temperature-sensitive growth defect, suggesting that Eco1 or cohesins respond to hyperthermic stress through a mechanism that occurs independent of Rad61. Here, we report that deletion of the G1 cyclin CLN2 rescues the temperature-sensitive lethality otherwise exhibited by eco1 rad61 mutant cells, such that the triple mutant cells exhibit robust growth over a broad range of temperatures. While Cln1, Cln2, and Cln3 are functionally redundant G1 cyclins, neither CLN1 nor CLN3 deletions rescue the temperature-sensitive growth defects otherwise exhibited by eco1 rad61 double mutants. We further provide evidence that CLN2 deletion rescues hyperthermic growth defects independent of START and impacts the state of chromosome condensation. These findings reveal novel roles for Cln2 that are unique among the G1 cyclin family and appear critical for cohesin regulation during hyperthermic stress.
登录
查看更多内容
粘着蛋白突变是合成的致命，并刺激Wnt信号传导。
影响因子：
7.7
作者：
Chin CV;Antony J;Ketharnathan S;Labudina A;Gimenez G;Parsons KM;He J;George AJ;Pallotta MM;Musio A;Braithwaite A;Guilford P;Hannan RD;Horsfield JA
通讯作者：
Horsfield JA
DOI：
10.1083/jcb.200605074
发表时间：
2006-08-14
期刊：
The Journal of cell biology
影响因子：
--
作者：
Ding DQ;Sakurai N;Katou Y;Itoh T;Shirahige K;Haraguchi T;Hiraoka Y
通讯作者：
Hiraoka Y
影响因子：
1.2
作者：
Cingolani, Pablo;Platts, Adrian;Ruden, Douglas M.
通讯作者：
Ruden, Douglas M.
影响因子：
2.4
作者：
Banerji R;Skibbens RV;Iovine MK
通讯作者：
Iovine MK
影响因子：
50.3
作者：
Adane B;Alexe G;Seong BKA;Lu D;Hwang EE;Hnisz D;Lareau CA;Ross L;Lin S;Dela Cruz FS;Richardson M;Weintraub AS;Wang S;Iniguez AB;Dharia NV;Conway AS;Robichaud AL;Tanenbaum B;Krill-Burger JM;Vazquez F;Schenone M;Berman JN;Kung AL;Carr SA;Aryee MJ;Young RA;Crompton BD;Stegmaier K
通讯作者：
Stegmaier K