Max Planck Institute of Molecular Cell Biology and Genetics, Pfotenhauerstraße 108, 01307 Dresden, Germany.
Department of Biology, University of Massachusetts Boston, Integrated Sciences Complex, 100 Morrissey Boulevard, Boston, MA 02125, USA.
Biomolecules. 2022 Aug 6;12(8):1083. doi: 10.3390/biom12081083.
The requirement of vitamin A for the synthesis of the visual chromophore and the light-sensing pigments has been studied in vertebrate and invertebrate model organisms. To identify the molecular mechanisms that orchestrate the ocular response to vitamin A deprivation, we took advantage of the fact that predominantly requires vitamin A for vision, but not for development or survival. We analyzed the impacts of vitamin A deficiency on the morphology, the lipidome, and the proteome of the eye. We found that chronic vitamin A deprivation damaged the light-sensing compartments and caused a dramatic loss of visual pigments, but also decreased the molar abundance of most phototransduction proteins that amplify and transduce the visual signal. Unexpectedly, vitamin A deficiency also decreased the abundances of specific subunits of mitochondrial TCA cycle and respiratory chain components but increased the levels of cuticle- and lens-related proteins. In contrast, we found no apparent effects of vitamin A deficiency on the ocular lipidome. In summary, chronic vitamin A deficiency decreases the levels of most components of the visual signaling pathway, but also affects molecular pathways that are not vision-specific and whose mechanistic connection to vitamin A remains to be elucidated.
维生素 A 对于视觉色素和感光色素的合成的需求，已经在脊椎动物和无脊椎动物模型生物中进行了研究。为了确定调控眼部对维生素 A 缺乏反应的分子机制，我们利用了这样一个事实，即 主要需要维生素 A 来维持视觉，但不需要其来发育或生存。我们分析了维生素 A 缺乏对 眼睛的形态、脂质组和蛋白质组的影响。我们发现，慢性维生素 A 缺乏会破坏感光区，并导致视觉色素的急剧丧失，但也降低了放大和转导视觉信号的大多数光转导蛋白的摩尔丰度。出乎意料的是，维生素 A 缺乏还降低了线粒体三羧酸循环和呼吸链成分的特定亚基的丰度，但增加了与甲壳质和晶状体相关的蛋白质的水平。相比之下，我们没有发现维生素 A 缺乏对眼部脂质组有明显的影响。总之，慢性维生素 A 缺乏会降低视觉信号通路的大多数成分的水平，但也会影响不是专门针对视觉的分子途径，其与维生素 A 的机制联系仍有待阐明。
