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脂质重塑调节剂 1(LRL1)在莱茵衣藻的磷饥饿响应中与 PSR1 的作用不同。

Lipid remodeling regulator 1 (LRL1) is differently involved in the phosphorus-depletion response from PSR1 in Chlamydomonas reinhardtii.

机构信息

Graduate School of Bioscience and Biotechnology, Tokyo Institute of Technology, 4259-B-65 Nagatsuta-cho, Midori-ku, Yokohama, 226-8501, Japan.

School of Life Science and Technology, Tokyo Institute of Technology, 4259-B-65 Nagatsuta-cho, Midori-ku, Yokohama, 226-8501, Japan.

出版信息

Plant J. 2019 Nov;100(3):610-626. doi: 10.1111/tpj.14473. Epub 2019 Aug 23.

Abstract

The elucidation of lipid metabolism in microalgae has attracted broad interest, as their storage lipid, triacylglycerol (TAG), can be readily converted into biofuel via transesterification. TAG accumulates in the form of oil droplets, especially when cells undergo nutrient deprivation, such as for nitrogen (N), phosphorus (P), or sulfur (S). TAG biosynthesis under N-deprivation has been comprehensively studied in the model microalga Chlamydomonas reinhardtii, during which TAG accumulates dramatically. However, the resulting rapid breakdown of chlorophyll restricts overall oil yield productivity and causes cessation of cell growth. In contrast, P-deprivation results in oil accumulation without disrupting chloroplast integrity. We used a reverse genetics approach based on co-expression analysis to identify a transcription factor (TF) that is upregulated under P-depleted conditions. Transcriptomic analysis revealed that the mutants showed repression of genes typically associated with lipid remodeling under P-depleted conditions, such as sulfoquinovosyl diacylglycerol 2 (SQD2), diacylglycerol acyltransferase (DGTT1), and major lipid droplet protein (MLDP). As accumulation of sulfoquinovosyl diacylglycerol and TAG were suppressed in P-depleted mutants, we designated the protein as lipid remodeling regulator 1 (LRL1). LRL1 mutants showed slower growth under P-depletion. Moreover, cell size in the mutant was significantly reduced, and TAG and starch accumulation per cell were decreased. Transcriptomic analysis also suggested the repression of several genes typically upregulated in adaptation to P-depletion that are associated with the cell cycle and P and lipid metabolism. Thus, our analysis of LRL1 provides insights into P-allocation and lipid remodeling under P-depleted conditions in C. reinhardtii. OPEN RESEARCH BADGES: This article has earned an Open Data Badge for making publicly available the digitally-shareable data necessary to reproduce the reported results. The sequencing data were made publicly available under the BioProject Accession number PRJDB6733 and an accession number LC488724 at the DNA Data Bank of Japan (DDBJ). The data is available at https://trace.ddbj.nig.ac.jp/BPSearch/bioproject?acc=PRJDB6733; http://getentry.ddbj.nig.ac.jp/getentry/na/LC488724. The metabolome data were made publicly available and can be accessed at http://metabolonote.kazusa.or.jp/SE195:/; http://webs2.kazusa.or.jp/data/nur/.

摘要

阐明微藻中的脂质代谢引起了广泛的关注,因为它们的储存脂质三酰基甘油(TAG)可以通过酯交换很容易转化为生物燃料。TAG 以油滴的形式积累,特别是当细胞经历营养剥夺时,如氮(N)、磷(P)或硫(S)。在模式微藻莱茵衣藻中,对氮饥饿下的 TAG 生物合成进行了全面研究,在此期间,TAG 大量积累。然而,由此导致的叶绿素迅速分解限制了整体油产量的生产力,并导致细胞生长停止。相比之下,磷饥饿导致油的积累而不破坏叶绿体的完整性。我们使用基于共表达分析的反向遗传学方法来鉴定在磷饥饿条件下上调的转录因子(TF)。转录组分析表明,突变体显示出在磷饥饿条件下通常与脂质重塑相关的基因受到抑制,例如磺基奎诺二酰甘油 2(SQD2)、二酰甘油酰基转移酶(DGTT1)和主要脂滴蛋白(MLDP)。由于磷饥饿突变体中磺基奎诺二酰甘油和 TAG 的积累受到抑制,我们将该蛋白命名为脂质重塑调节剂 1(LRL1)。LRL1 突变体在磷饥饿下生长较慢。此外,突变体的细胞大小显著减小,每个细胞的 TAG 和淀粉积累减少。转录组分析还表明,几个通常在适应磷饥饿时上调的与细胞周期和磷及脂质代谢相关的基因受到抑制。因此,我们对 LRL1 的分析提供了在莱茵衣藻中磷饥饿条件下磷分配和脂质重塑的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff76/6899820/9103c128db61/TPJ-100-610-g001.jpg

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