Liu Jianhua, Jia Yonghui, Li Juntao, Chu Zhaoqing
Ocean Research Centre of Zhoushan, Zhejiang University, 10 Tiyu Road, Room 502, Zhoushan, 310058, ZJ, China,
Mol Genet Genomics. 2015 Jun;290(3):1067-83. doi: 10.1007/s00438-014-0966-6. Epub 2014 Dec 21.
Nitrogen starvation (NS) induces sexual development when mating partners are available or enter into quiescent state (G0) in heterothallic background in fission yeast. However, little is known whether the two processes share common signaling molecules or cells defective in the two processes share common transcriptional signatures. To address these questions, we first assessed 77 kinase-deletion strains for NS-induced G0-arrest phenotypes. Our result indicated that 10 out of 77 kinase-deletion strains exhibited defect in G0-arrest, only 3 of which were defective in sexual development based on a previous study, suggesting that the two processes hardly share common signaling components. We subsequently performed transcriptional profiling analysis. Our result indicated that NS-induced transcriptional change was so robust that it prevailed the alteration by individual kinase-deletion alleles. Based on comparison between kinase-deletion strains proficient and deficient in sexual development or G0-arrest, we identified subsets of genes that were associated with sexual development-deficient or G0-arrest-deficient kinase-deletion strains. Multiple pairing analyses allowed grouping of functional related kinases. Furthermore, we showed that Pka1-mediated pathways were required for upregulation of NS-induced genes upon NS and downregulation of the same set of genes under the N-replete conditions. Taken together, our analyses indicate that sexual development and NS-induced G0-arrest are unrelated; and sexual development-deficient and G0-arrest-deficient kinase-deletion strains possess distinct transcriptional signatures. We propose that Pka1 is a key regulator of nitrogen metabolic pathways and Pka1-mediated signaling pathways play roles in regulation of NS-induced genes under both N-depleted and N-replete conditions.
在裂殖酵母的异宗配合背景下，当有交配伴侣时，氮饥饿（NS）会诱导有性生殖发育，否则进入静止状态（G0）。然而，对于这两个过程是否共享共同的信号分子，或者在这两个过程中存在缺陷的细胞是否共享共同的转录特征，我们知之甚少。为了解决这些问题，我们首先评估了77个激酶缺失菌株的NS诱导的G0期停滞表型。我们的结果表明，77个激酶缺失菌株中有10个在G0期停滞方面存在缺陷，根据之前的一项研究，其中只有3个在有性生殖发育方面存在缺陷，这表明这两个过程几乎不共享共同的信号成分。我们随后进行了转录谱分析。我们的结果表明，NS诱导的转录变化非常强烈，以至于它压倒了单个激酶缺失等位基因引起的变化。基于对有性生殖发育或G0期停滞方面有缺陷和无缺陷的激酶缺失菌株的比较，我们确定了与有性生殖发育缺陷或G0期停滞缺陷的激酶缺失菌株相关的基因子集。多重配对分析允许对功能相关的激酶进行分组。此外，我们表明，Pka1介导的途径对于NS诱导的基因在NS条件下的上调以及在氮充足条件下同一组基因的下调是必需的。综上所述，我们的分析表明，有性生殖发育和NS诱导的G0期停滞是不相关的；有性生殖发育缺陷和G0期停滞缺陷的激酶缺失菌株具有不同的转录特征。我们提出，Pka1是氮代谢途径的关键调节因子，并且Pka1介导的信号通路在氮缺乏和氮充足条件下对NS诱导基因的调节中发挥作用。
