School of Biological Sciences, Bangor University, Bangor, Gwynedd LL57 2UW, UK.
Biochem Soc Trans. 2010 Oct;38(5):1230-3. doi: 10.1042/BST0381230.
Mutation of the ACN1 (acetate non-utilizing 1) locus of Arabidopsis results in altered acetate assimilation into gluconeogenic sugars and anapleurotic amino acids and leads to an overall depression in primary metabolite levels by approx. 50% during seedling development. Levels of acetyl-CoA were higher in acn1 compared with wild-type, which is counterintuitive to the activity of ACN1 as a peroxisomal acetyl-CoA synthetase. We hypothesize that ACN1 recycles free acetate to acetyl-CoA within peroxisomes in order that carbon remains fed into the glyoxylate cycle. When ACN1 is not present, carbon in the form of acetate can leak out of peroxisomes and is reactivated to acetyl-CoA within the cytosol. Kinetic models incorporating estimates of carbon input and pathway dynamics from a variety of literature sources have proven useful in explaining how ACN1 may prevent the carbon leak and even contribute to the control of peroxisomal carbon metabolism.
拟南芥 ACN1（乙酸非利用 1）基因座的突变导致将乙酸同化到糖异生糖和氨酰基氨基酸的过程发生改变，并导致幼苗发育过程中初级代谢物水平总体下降约 50%。与野生型相比，acn1 中的乙酰辅酶 A 水平更高，这与 ACN1 作为过氧化物体乙酰辅酶 A 合成酶的活性相反。我们假设 ACN1 在过氧化物体中将游离乙酸循环回乙酰辅酶 A，以便碳仍然进入乙醛酸循环。当 ACN1 不存在时，以乙酸形式存在的碳可以从过氧化物体中漏出，并在细胞质中重新激活为乙酰辅酶 A。从各种文献来源中估算碳输入和途径动态的动力学模型已被证明有助于解释 ACN1 如何防止碳泄漏，甚至有助于控制过氧化物体碳代谢。
