Microalgae hold great promises as sustainable cellular factories for the production of alternative fuels, feeds, and biopharmaceuticals for human health. While the biorefinery approach for fuels along with the coproduction of high-value compounds with industrial, therapeutic, or nutraceutical applications have the potential to make algal biofuels more economically viable, a number of challenges continue to hamper algal production systems at all levels. One such hurdle includes the metabolic trade-off often observed between the increased yields of desired products, such as triacylglycerols (TAG), and the growth of an organism. Initial genetic engineering strategies to improve lipid productivity in microalgae, which focused on overproducing the enzymes involved in fatty acid and TAG biosynthesis or inactivating competing carbon (C) metabolism, have seen some successes albeit at the cost of often greatly reduced biomass. Emergent approaches that aim at modifying the dynamics of entire metabolic pathways by engineering of pertinent transcription factors or signaling networks appear to have successfully achieved a balance between growth and neutral lipid accumulation. However, the biological knowledge of key signaling networks and molecular components linking these two processes is still incomplete in photosynthetic eukaryotes, making it difficult to optimize metabolic engineering strategies for microalgae. Here, we focus on nitrogen (N) starvation of the model green microalga, Chlamydomonas reinhardtii, to present the current understanding of the nutrient-dependent switch between proliferation and quiescence, and the drastic reprogramming of metabolism that results in the storage of C compounds following N starvation. We discuss the potential components mediating the transcriptional repression of cell cycle genes and the establishment of quiescence in Chlamydomonas, and highlight the importance of signaling pathways such as those governed by the target of rapamycin (TOR) and sucrose nonfermenting-related (SnRK) kinases in the coordination of metabolic status with cellular growth. A better understanding of how the cell division cycle is regulated in response to nutrient scarcity and of the signaling pathways linking cellular growth to energy and lipid homeostasis, is essential to improve the prospects of biofuels and biomass production in microalgae.

中文翻译：

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衣藻中氮依赖的细胞周期，静止和TAG积累的协调。

作为可持续发展的蜂窝工厂，微藻有望为人类健康生产代用燃料，饲料和生物制药。尽管燃料的生物精炼方法以及与工业，治疗或营养保健应用联产的高价值化合物具有使藻类生物燃料在经济上更可行的潜力，但许多挑战仍在继续阻碍藻类生产系统的各个层面。一个这样的障碍包括经常在所需产物例如三酰基甘油（TAG）的产量增加与生物体生长之间观察到的代谢折衷。旨在提高微藻类脂质生产率的初步基因工程策略，其重点是过量生产参与脂肪酸和TAG生物合成或使竞争性碳（C）代谢失活的酶，已经取得了一些成功，尽管是以经常减少生物量为代价的。旨在通过工程化相关转录因子或信号网络来修饰整个代谢途径动力学的新兴方法似乎已成功地实现了生长与中性脂质蓄积之间的平衡。然而，在光合作用的真核生物中，关键信号网络和连接这两个过程的分子成分的生物学知识仍然不完整，因此难以优化微藻的代谢工程策略。在这里，我们重点关注绿色微藻模型衣藻（Chlamydomonas reinhardtii）的氮（N）饥饿状况，以介绍当前对增生与静止之间营养素依赖性转换的了解，以及新陈代谢的剧烈重编程，导致N饥饿后C化合物的储存。我们讨论介导细胞周期基因转录抑制和衣藻的静止建立的潜在组成部分，并强调信号转导通路的重要性，例如雷帕霉素（TOR）和蔗糖非发酵相关（SnRK）激酶的靶标控制的那些代谢状态与细胞生长的协调。更好地理解如何响应营养缺乏和如何调节细胞分裂周期以及将细胞生长与能量和脂质稳态联系起来的信号通路，对于改善微藻中生物燃料和生物质生产的前景至关重要。我们讨论了介导细胞周期基因转录抑制和衣原体静止的建立的潜在组成部分，并强调了信号通路的重要性，例如受雷帕霉素（TOR）和蔗糖非发酵相关（SnRK）激酶靶标控制的那些信号通路。代谢状态与细胞生长的协调。更好地理解如何响应营养缺乏和如何调节细胞分裂周期以及将细胞生长与能量和脂质稳态联系起来的信号通路，对于改善微藻中生物燃料和生物质生产的前景至关重要。我们讨论介导细胞周期基因转录抑制和衣藻的静止建立的潜在组成部分，并强调信号转导通路的重要性，例如受雷帕霉素（TOR）和蔗糖非发酵相关（SnRK）激酶靶标控制的那些通路代谢状态与细胞生长的协调。更好地理解如何响应营养缺乏和如何调节细胞分裂周期以及将细胞生长与能量和脂质稳态联系起来的信号通路，对于改善微藻中生物燃料和生物质生产的前景至关重要。并强调了信号通路的重要性，例如受雷帕霉素（TOR）和蔗糖非发酵相关（SnRK）激酶靶标调控的信号通路在代谢状态与细胞生长协调中的重要性。更好地理解如何响应营养缺乏和如何调节细胞分裂周期以及将细胞生长与能量和脂质稳态联系起来的信号通路，对于改善微藻中生物燃料和生物质生产的前景至关重要。并强调了信号通路的重要性，例如受雷帕霉素（TOR）和蔗糖非发酵相关（SnRK）激酶靶标调控的信号通路在代谢状态与细胞生长协调中的重要性。更好地理解如何响应营养缺乏和如何调节细胞分裂周期以及将细胞生长与能量和脂质稳态联系起来的信号通路，对于改善微藻中生物燃料和生物质生产的前景至关重要。