AMINO ACID DEPRIVATION‐INDUCED EXPRESSION OF ASPARAGINE SYNTHETASE REGULATES THE GROWTH AND SURVIVAL OF CULTURED SILKWORM CELLS. Issue 2 (30th April 2013)

• Record Type: Journal Article
• Authors: Li, Zhiqing; Zhu, Li; Xu, Jian; Mon, Hiroaki; Lee, Jae Man; Kusakabe, Takahiro
• Is Part Of: Archives of insect biochemistry and physiology. Volume 83:Issue 2(2013:Jun.)
• Page Start: 57
• Page End: 68
• Publication Date: 2013-04-30
• Subjects: Insects -- Physiology -- Periodicals; Insect biochemistry -- Periodicals; 595.701572
• DOI: 10.1002/arch.21091
• Languages: English
• ISSNs: 0739-4462

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <p>Expression of <italic>Bombyx mori Asparagine synthetase</italic> (<italic>BmASNS</italic>), one gene that encodes an enzyme catalyzing asparagine biosynthesis, is transcriptionally induced following amino acid deprivation. Previous transcriptional analysis of the <italic>BmASNS</italic> gene showed the involvement of Polycomb proteins, epigenetic repressors, in suppressing <italic>BmASNS</italic> expression in a cell cycle‐dependent manner. However, the role of BmAsns protein in these cellular processes remains unclear. The present study thus exploited the potential function of BmAsns protein in cultured silkworm cells. Our results showed that ectopic overexpression of <italic>BmASNS</italic> gene effectively inhibited cell growth in silkworm cells, whereas its overexpression could rescue cell growth upon amino acid deprivation treatment. We found that the cells expressing BmAsns protein were capable of influencing the formation of autophagic vacuoles stimulated by amino acid deprivation. We speculated that the recovery of cell growth by overexpressed BmAsns protein is due to the rapid turnover of autophagic vacuoles in the cells. To further assess the effects of BmAsns on cell development, we used RNA interference to silence <italic>BmASNS</italic> expression in silkworm cells in the presence or absence of amino acids. Our results revealed a significant change of cell proliferation as well as cell cycle distribution after knockdown of <italic>BmASNS</italic>. Importantly, silkworm cells lacking <italic>BmASNS</italic> under the condition of amino acid deprivation showed severely impaired proliferation. Altogether, we concluded that the up‐regulated expression of <italic>BmASNS</italic> would be able to protect cells from impairment induced by amino acid deprivation, which in turn facilitates cell growth and survival.</p> </abstract>