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锰通过 DAF-16 转录因子激活和线虫卵黄蛋白原下调的可逆生殖毒性作用。

Reversible reprotoxic effects of manganese through DAF-16 transcription factor activation and vitellogenin downregulation in Caenorhabditis elegans.

机构信息

Departamento de Química, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil.

Institute of Nutritional Sciences, University of Potsdam, Arthur-Scheunert-Allee 114-166, 14558 Nuthetal, Germany.

出版信息

Life Sci. 2016 Apr 15;151:218-223. doi: 10.1016/j.lfs.2016.03.016. Epub 2016 Mar 10.

Abstract

AIMS

Vitellogenesis is the yolk production process which provides the essential nutrients for the developing embryos. Yolk is a lipoprotein particle that presents lipids and lipid-binding proteins, referred to as vitellogenins (VIT). The Caenorhabditis elegans nematode has six genes encoding VIT lipoproteins. Several pathways are known to regulate vitellogenesis, including the DAF-16 transcription factor. Some reports have shown that heavy metals, such as manganese (Mn), impair brood size in C. elegans; however the mechanisms associated with this effect have yet to be identified. Our aim was to evaluate Mn's effects on C. elegans reproduction and better understand the pathways related to these effects.

MAIN METHODS

Young adult larval stage worms were treated for 4h with Mn in 85mM NaCl and Escherichia coli OP50 medium.

KEY FINDINGS

Mn reduced egg-production and egg-laying during the first 24h after the treatment, although the total number of progenies were indistinguishable from the control group levels. This delay may have occurred due to DAF-16 activation, which was noted only after the treatment and was not apparent 24h later. Moreover, the expression, protein levels and green fluorescent protein (GFP) fluorescence associated with VIT were decreased soon after Mn treatment and recovered after 24h.

SIGNIFICANCE

Combined, these data suggest that the delay in egg-production is likely regulated by DAF-16 and followed by the inhibition of VIT transport activity. Further studies are needed to clarify the mechanisms associated with Mn-induced DAF-16 activation.

摘要

目的

卵黄发生是卵黄生成的过程,为发育中的胚胎提供必需的营养物质。卵黄是一种脂蛋白颗粒,其中包含脂质和脂质结合蛋白,称为卵黄蛋白原(VIT)。秀丽隐杆线虫有 6 个编码 VIT 脂蛋白的基因。有几种途径已知可以调节卵黄发生,包括 DAF-16 转录因子。一些报道表明,重金属,如锰(Mn),会损害线虫的种群大小;然而,与这种效应相关的机制尚未确定。我们的目的是评估 Mn 对秀丽隐杆线虫生殖的影响,并更好地理解与这些影响相关的途径。

主要方法

用 Mn 在 85mM NaCl 和大肠杆菌 OP50 培养基中处理处于年轻成虫阶段的幼虫 4 小时。

主要发现

Mn 减少了处理后 24 小时内的产卵量和产卵量,尽管总后代数量与对照组水平无明显差异。这种延迟可能是由于 DAF-16 的激活引起的,仅在处理后才注意到,24 小时后并不明显。此外,VIT 的表达、蛋白水平和绿色荧光蛋白(GFP)荧光在 Mn 处理后很快下降,并在 24 小时后恢复。

意义

综上所述,这些数据表明,产卵的延迟可能受到 DAF-16 的调节,并随后抑制 VIT 转运活性。需要进一步研究来阐明与 Mn 诱导的 DAF-16 激活相关的机制。

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