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构巢曲霉bncA1突变导致细胞分裂周期、核运动和发育形态发生出现缺陷。

The Aspergillus nidulans bncA1 mutation causes defects in the cell division cycle, nuclear movement and developmental morphogenesis.

作者信息

Castiglioni Pascon R, Pizzirani-Kleiner A A, Miller B L

机构信息

Department of Microbiology, Molecular Biology and Biochemistry, University of Idaho, Moscow 83844, USA.

出版信息

Mol Gen Genet. 2001 Jan;264(5):546-54. doi: 10.1007/s004380000360.

DOI:10.1007/s004380000360
PMID:11212909
Abstract

Wild-type Aspergillus nidulans conidia are uninucleate. The mutation bncA1 (binucleated conidia) was first described as a single mutation located on chromosome IV that caused formation of approximately 25% binucleate and 1% trinucleate conidia. In this study, we show that bncA1 conidia exit G1 arrest earlier than the wild type. Germlings have hyphal elements with abnormal morphology, elevated numbers of randomly distributed nuclei and an irregular septation pattern. Older hyphal elements undergo mitotic catastrophe, suggesting the nuclear division cycle of internal (nonterminal) elements is not arrested. The bncA1 mutation also causes aberrant morphogenesis of the asexual reproductive structure, the conidiophore. Metulae and phialides are elongated and have incorrect numbers of nuclei. Phialides also have internal septation that appears to delineate hyphal-like elements. Heterokaryon analysis using strains with contrasting auxotrophic markers showed that the bncA1 mutation resulted in a higher frequency of diploid and multinucleated prototrophic conidia than control heterokaryons. These results suggest that in bncA1 strains multiple nuclei can move from the conidiophore vesicle to the metulae and/or from the phialide to the conidium. The bncA1 mutant also showed hypersensitivity to the anti-microtubule drugs thiabendazole and nocodazole, which is consistent with the defects in cell cycle regulation and nuclear movement. We propose that bncA has an important role in correctly regulating both the cell division cycle and nuclear movement.

摘要

野生型构巢曲霉分生孢子是单核的。bncA1(双核分生孢子)突变最初被描述为位于第四条染色体上的单个突变,该突变导致约25%的双核和1%的三核分生孢子形成。在本研究中,我们发现bncA1分生孢子比野生型更早地退出G1期停滞。芽管具有形态异常的菌丝成分、随机分布的细胞核数量增加以及不规则的隔膜模式。较老的菌丝成分会发生有丝分裂灾难,这表明内部(非末端)成分的核分裂周期没有停滞。bncA1突变还会导致无性繁殖结构分生孢子梗的异常形态发生。小梗和产孢细胞伸长,细胞核数量不正确。产孢细胞也有内部隔膜,似乎勾勒出类似菌丝的成分。使用具有不同营养缺陷型标记的菌株进行异核体分析表明,与对照异核体相比,bncA1突变导致二倍体和多核原养型分生孢子的频率更高。这些结果表明,在bncA1菌株中,多个细胞核可以从分生孢子梗囊泡移动到小梗和/或从产孢细胞移动到分生孢子。bncA1突变体对抗微管药物噻苯咪唑和诺考达唑也表现出超敏感性,这与细胞周期调控和核移动的缺陷一致。我们提出bncA在正确调节细胞分裂周期和核移动方面具有重要作用。

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The Aspergillus nidulans bncA1 mutation causes defects in the cell division cycle, nuclear movement and developmental morphogenesis.构巢曲霉bncA1突变导致细胞分裂周期、核运动和发育形态发生出现缺陷。
Mol Gen Genet. 2001 Jan;264(5):546-54. doi: 10.1007/s004380000360.
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Characterization of an Aspergillus nidulans mutant with abnormal distribution of nuclei in hyphae, metulae, phialides and conidia.构巢曲霉一个突变体的特征分析,该突变体在菌丝、小梗、产孢瓶体和分生孢子中细胞核分布异常。
FEMS Microbiol Lett. 1998 Sep 1;166(1):49-55. doi: 10.1111/j.1574-6968.1998.tb13182.x.
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Mutants of Aspergillus nidulans deficient in nuclear migration during hyphal growth and conidiation.在菌丝生长和分生孢子形成过程中核迁移存在缺陷的构巢曲霉突变体。
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hyp loci control cell pattern formation in the vegetative mycelium of Aspergillus nidulans.hyp基因座控制构巢曲霉营养菌丝体中的细胞模式形成。
Genetics. 1998 Feb;148(2):669-80. doi: 10.1093/genetics/148.2.669.
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hymA (hypha-like metulae), a new developmental mutant of Aspergillus nidulans.
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abaA controls phialide differentiation in Aspergillus nidulans.abaA基因控制构巢曲霉中瓶梗的分化。
Plant Cell. 1990 Aug;2(8):731-9. doi: 10.1105/tpc.2.8.731.
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The Aspergillus nidulans putative kinase, KfsA (kinase for septation), plays a role in septation and is required for efficient asexual spore formation.构巢曲霉假定激酶KfsA(隔膜形成激酶)在隔膜形成过程中发挥作用,是高效无性孢子形成所必需的。
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Evidence that the Aspergillus nidulans class I and class II chitin synthase genes, chsC and chsA, share critical roles in hyphal wall integrity and conidiophore development.构巢曲霉I类和II类几丁质合成酶基因chsC和chsA在菌丝壁完整性和分生孢子梗发育中发挥关键作用的证据。
J Biochem. 2000 Mar;127(3):359-66. doi: 10.1093/oxfordjournals.jbchem.a022616.

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