Nuclear kernel stress affects lipid metabolism: activate transcription factor PHA-4/FoxA.

Lipid droplets are important organelles and are essential for maintaining normal cellular energy metabolism and physiological function.
lipid droplets interact with other organelles, respond to changes in the internal and external environment of the cell, and dynamically regulate the cell's lipid metabolism and energy balance.
when the function of the organ changes, it not only causes the organ stress reaction (e.g. endoscopic non-folding protein reaction, mitochondrial non-folding protein reaction), but also leads to changes in energy metabolism (obesity, diabetes, fatty liver and other metabolic diseases).
in eukaryotes, the main function of the nucleosome is ribosome biogenesis, including rDNA transcription, rRNA synthesis, processing, and the assembly of ribosome subunits.
when the process of rnacosic organisms is disturbed or destroyed, the cells enter a state of nucleolus stress.
has been shown that nucleosome stress can cause the activation of the anti-cancer gene p53, which inhibits the cell cycle and even promotes apoptosis to adapt to nuclear renition stress.
but the bio-occurrence of ribosomes is a very energy-intensive biological process in cells, so does kernel stress affect lipid metabolism? Pattern biological lysisis are widely used in various fields of life science research.
using the advantages of whole genome genetic screening of the whole genome of the Chinese Academy of Sciences, Liang Bin, a researcher at kunming Zoology Institute of the Chinese Academy of Sciences, looked for genes or signaling pathways that affect the size of lipid droplets and fat storage, and found that the rpm-8 gene mutation showed significant increase in lipid droplets and excessive accumulation of fat.
rrp-8 is mainly involved in the preprocessing processing of rRNA, which causes the synthesis of ribosomes to be significantly inhibited by mutation. further research
found that, similar to the rrp-8 gene mutant phenotype, whether it is the use of anti-mycin D (Actinomycin D) to inhibit rDNA transcription, or pro-2/pro-3 and other mutant nematodes involved in rRNA processing, there will be increased lipid droplets and excessive accumulation of fat, indicating that nucleoin stress changes energy metabolism, resulting in the accumulation of fat.
study also found that the accumulation of fat caused by nuclear stress did not depend on the known transcription factor P53 protein, but rather on another transcription factor fork protein FoxA/PHA-4.
nucleosome stress through the ribosome protein RPL11/RPL5, increase the PHA-4 expression located in the nucleus, transcription activates the expression of fat synthesis gene, promotes fat synthesis and accumulation.
it is worth noting that the accumulation of fat caused by nuclear kernel stress is beneficial to the beauty nematodes against hunger.
the new study found a correlation between organ stress and lipid metabolism, the nuclear kernel stress activated transcription factor PHA-4/FoxA, which increases fat synthesis and converts energy into fat storage.
research results from FOXA/PHA-4 Senses Nucleolar Stress to Regulate Authority in Caenorhabditis elegans, published in Nature-Communications, with Wu Jieyu, APh. dr., Jiang Xue, co-first author of the paper, liang Bin and Kunming College Professor Yu Xiaoju as co-authors.
the research has been supported by the Chinese Academy of Sciences' strategic leading science and technology special (B), the National Natural Science Foundation, Yunnan Province high-end scientific and technological personnel, Yunnan Province, young and middle-aged academic reserve talents and other projects.
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