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The lin-4 gene controls fat accumulation and longevity in Caenorhabditis elegans.

Zhu C, Ji CB, Zhang CM, Gao CL, Zhu JG, Qin DN, Kou CZ, Zhu GZ, Shi CM, Guo XR - Int J Mol Sci (2010)

Bottom Line: In this study, we showed that the fat content is reduced remarkably in C. elegans lin-4 mutants.We also showed that lin-4 mutants have a significantly shorter life span than wild-type worms.DCF assay experiments showed that the reactive oxygen species (ROS) levels increased and mitochondrial DNA (mtDNA) copy number decreased in loss-of-function lin-4 mutants.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, Nanjing Maternal and Child Health Hospital of Nanjing Medical University, No.123 Tianfei Road, 210004 Nanjing, China; E-Mails: zhifangxibao@163.com (C.Z.); zhangcm79@163.com (C.-M.Z.).

ABSTRACT
Previous studies have determined that lin-4, which was the first miRNA to be discovered, controls the timing of cell fate determination and life span in Caenorhabditis elegans. However, the mechanism of lin-4 involvement in these processes remains poorly understood. Fat storage is an essential aspect of the life cycle of organisms, and the function of lin-4 in fat accumulation is not clear. In this study, we showed that the fat content is reduced remarkably in C. elegans lin-4 mutants. Quantitative RT-PCR analysis revealed a considerable decrease in the levels of SBP-1 and OGA-1 mRNA in lin-4 mutants. We also showed that lin-4 mutants have a significantly shorter life span than wild-type worms. DCF assay experiments showed that the reactive oxygen species (ROS) levels increased and mitochondrial DNA (mtDNA) copy number decreased in loss-of-function lin-4 mutants. These mutants also showed attenuation of locomotion. Taken together, our findings suggest that lin-4 may play an important role in regulating fat accumulation and locomotion and that lin-4 may control the life span of C. elegans by mediating ROS production.

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Related in: MedlinePlus

The effect of lin-4 on ROS level. (A) Intracellular ROS in C. elegans were measured using 2,7-dichlorofluorescein diacetate (DCF-DA; Molecular Probes). Sixty animals from each group were analyzed (n = 60). Scale bar: 100 μm; (B) results are expressed as mean ± SD of relative fluorescence units (RFU). * p < 0.05.
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f3-ijms-11-04814: The effect of lin-4 on ROS level. (A) Intracellular ROS in C. elegans were measured using 2,7-dichlorofluorescein diacetate (DCF-DA; Molecular Probes). Sixty animals from each group were analyzed (n = 60). Scale bar: 100 μm; (B) results are expressed as mean ± SD of relative fluorescence units (RFU). * p < 0.05.

Mentions: DCF assay experiments revealed that worms with a loss-of-function mutation in lin-4 showed ROS accumulation (Figure 3). We examined the mtDNA copy number in lin-4 mutants and wild-type animals by performing real-time PCR. The mtDNA copy number in lin-4 mutants was significantly lower than that in the wild-type control (Figure 4).


The lin-4 gene controls fat accumulation and longevity in Caenorhabditis elegans.

Zhu C, Ji CB, Zhang CM, Gao CL, Zhu JG, Qin DN, Kou CZ, Zhu GZ, Shi CM, Guo XR - Int J Mol Sci (2010)

The effect of lin-4 on ROS level. (A) Intracellular ROS in C. elegans were measured using 2,7-dichlorofluorescein diacetate (DCF-DA; Molecular Probes). Sixty animals from each group were analyzed (n = 60). Scale bar: 100 μm; (B) results are expressed as mean ± SD of relative fluorescence units (RFU). * p < 0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC3100830&req=5

f3-ijms-11-04814: The effect of lin-4 on ROS level. (A) Intracellular ROS in C. elegans were measured using 2,7-dichlorofluorescein diacetate (DCF-DA; Molecular Probes). Sixty animals from each group were analyzed (n = 60). Scale bar: 100 μm; (B) results are expressed as mean ± SD of relative fluorescence units (RFU). * p < 0.05.
Mentions: DCF assay experiments revealed that worms with a loss-of-function mutation in lin-4 showed ROS accumulation (Figure 3). We examined the mtDNA copy number in lin-4 mutants and wild-type animals by performing real-time PCR. The mtDNA copy number in lin-4 mutants was significantly lower than that in the wild-type control (Figure 4).

Bottom Line: In this study, we showed that the fat content is reduced remarkably in C. elegans lin-4 mutants.We also showed that lin-4 mutants have a significantly shorter life span than wild-type worms.DCF assay experiments showed that the reactive oxygen species (ROS) levels increased and mitochondrial DNA (mtDNA) copy number decreased in loss-of-function lin-4 mutants.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, Nanjing Maternal and Child Health Hospital of Nanjing Medical University, No.123 Tianfei Road, 210004 Nanjing, China; E-Mails: zhifangxibao@163.com (C.Z.); zhangcm79@163.com (C.-M.Z.).

ABSTRACT
Previous studies have determined that lin-4, which was the first miRNA to be discovered, controls the timing of cell fate determination and life span in Caenorhabditis elegans. However, the mechanism of lin-4 involvement in these processes remains poorly understood. Fat storage is an essential aspect of the life cycle of organisms, and the function of lin-4 in fat accumulation is not clear. In this study, we showed that the fat content is reduced remarkably in C. elegans lin-4 mutants. Quantitative RT-PCR analysis revealed a considerable decrease in the levels of SBP-1 and OGA-1 mRNA in lin-4 mutants. We also showed that lin-4 mutants have a significantly shorter life span than wild-type worms. DCF assay experiments showed that the reactive oxygen species (ROS) levels increased and mitochondrial DNA (mtDNA) copy number decreased in loss-of-function lin-4 mutants. These mutants also showed attenuation of locomotion. Taken together, our findings suggest that lin-4 may play an important role in regulating fat accumulation and locomotion and that lin-4 may control the life span of C. elegans by mediating ROS production.

Show MeSH
Related in: MedlinePlus