DHS-21, a dicarbonyl/<scp>l</scp>
-xylulose reductase (DCXR) ortholog, regulates longevity and reproduction in <i>Caenorhabditis elegans</i>

Son, Le Tho; Ko, Kyung-Min; Cho, Jeong Hoon; Singaravelu, Gunasekaran; Chatterjee, Indrani; Choi, Tae-Woo; Song, Hyun-Ok; Yu, Jae-Ran; Park, Byung-Jae; Lee, Sun-Kyung; Ahnn, Joohong

doi:10.1016/j.febslet.2011.03.062

Cited by 10 publications

(2 citation statements)

References 17 publications

(31 reference statements)

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“…Standard western blot analysis was performed from whole-nematode crude protein extracts prepared by bead beating from mixed-stage cultures of WT and xpa-1 using the following primary antibodies: rabbit anti-alpha actin (Abcam) or rabbit anti-Sti-1/Hop (27) or rabbit anti-DHS-21 (28), provided by Klaus Richter (Technische Universität München, Garching, Germany) and Joohong Ahnn (Hanyang University, Republic of Korea), respectively. Evaluation of P gst-4::gfp transgene expression was performed on whole-nematode protein extracts prepared from ∼200 adult CL2166 nematode, the P gst-4::gfp transgene expression was measured relative to actin by western blot analysis using anti-GFP (Clontech) and anti-actin (Sigma) as primary antibodies followed by quantification using ImageJ.…”

Section: Methodsmentioning

confidence: 99%

Active transcriptomic and proteomic reprogramming in the C. elegans nucleotide excision repair mutant xpa-1

Arczewska

Tomazella

Lindvall

et al. 2013

Nucleic Acids Research

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Transcription-blocking oxidative DNA damage is believed to contribute to aging and to underlie activation of oxidative stress responses and down-regulation of insulin-like signaling (ILS) in Nucleotide Excision Repair (NER) deficient mice. Here, we present the first quantitative proteomic description of the Caenorhabditis elegans NER-defective xpa-1 mutant and compare the proteome and transcriptome signatures. Both methods indicated activation of oxidative stress responses, which was substantiated biochemically by a bioenergetic shift involving increased steady-state reactive oxygen species (ROS) and Adenosine triphosphate (ATP) levels. We identify the lesion-detection enzymes of Base Excision Repair (NTH-1) and global genome NER (XPC-1 and DDB-1) as upstream requirements for transcriptomic reprogramming as RNA-interference mediated depletion of these enzymes prevented up-regulation of genes over-expressed in the xpa-1 mutant. The transcription factors SKN-1 and SLR-2, but not DAF-16, were identified as effectors of reprogramming. As shown in human XPA cells, the levels of transcription-blocking 8,5'-cyclo-2'-deoxyadenosine lesions were reduced in the xpa-1 mutant compared to the wild type. Hence, accumulation of cyclopurines is unlikely to be sufficient for reprogramming. Instead, our data support a model where the lesion-detection enzymes NTH-1, XPC-1 and DDB-1 play active roles to generate a genomic stress signal sufficiently strong to result in transcriptomic reprogramming in the xpa-1 mutant.

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Section: Methodsmentioning

confidence: 99%

Active transcriptomic and proteomic reprogramming in the C. elegans nucleotide excision repair mutant xpa-1

Arczewska

Tomazella

Lindvall

et al. 2013

Nucleic Acids Research

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“…DCXR is a multifunctional protein involved in sugar metabolism, carbonyl detoxification, cell adhesion, and male fertility (34). C. elegans ortholog of DCXR (DHS-21) plays a role in detoxification of carbonyl compounds, and dhs-21 mutants have shorter lifespans presumably due to decreased defense against oxidative damage (77). Dcxr -deficient mice die before wean age, thus the role of DXCR in ovaries and female fertility was not assessed (76).…”

Section: Discussionmentioning

confidence: 99%

Single-cell and bulk transcriptional profiling of mouse ovaries reveals novel genes and pathways associated with DNA damage response in oocytes

Mills,

Emori,

Kumar

et al. 2024

Preprint

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Immature oocytes enclosed in primordial follicles stored in female ovaries are under constant threat of DNA damage induced by endogenous and exogenous factors. Checkpoint kinase 2 (CHEK2) is a key mediator of the DNA damage response in all cells. Genetic studies have shown that CHEK2 and its downstream targets, p53 and TAp63, regulate primordial follicle elimination in response to DNA damage, however the mechanism leading to their demise is still poorly characterized. Single-cell and bulk RNA sequencing were used to determine the DNA damage response in wildtype and Chek2-deficient ovaries. A low but oocyte-lethal dose of ionizing radiation induces a DNA damage response in ovarian cells that is solely dependent on CHEK2. DNA damage activates multiple ovarian response pathways related to apoptosis, p53, interferon signaling, inflammation, cell adhesion, and intercellular communication. These pathways are differentially employed by different ovarian cell types, with oocytes disproportionately affected by radiation. Novel genes and pathways are induced by radiation specifically in oocytes, shedding light on their sensitivity to DNA damage, and implicating a coordinated response between oocytes and pre-granulosa cells within the follicle. These findings provide a foundation for future studies on the specific mechanisms regulating oocyte survival in the context of aging, as well as therapeutic and environmental genotoxic exposures.

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The Same or Not the Same: Lineage-Specific Gene Expansions and Homology Relationships in Multigene Families in Nematodes

2014

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Homology is a fundamental concept in comparative biology and a crucial tool for the analysis of character distribution. Introduced by Owen in 1843 (Lectures on comparative anatomy and physiology of the invertebrate animals, Longman, Brown, Green and Longman, London) in a morphological context, homology can similarly be applied to protein-coding genes. However, in molecular biology the proper distinction between orthology and paralogy was long limited by the absence of whole-genome sequencing data. By now, genome-wide sequencing allows comprehensive analyses of the homology of genes and gene families at the level of an entire phylum. Here, we analyze a manually curated dataset of more than 2,000 proteins from the genomes of 11 nematode species of seven different genera, including free-living and animal and plant parasites to study the principles of homology assignments in gene families. Using all sequenced species as an extensive outgroup, we specifically focus on the two model species Caenorhabditis elegans and Pristionchus pacificus and compare enzymes involved in detoxification of xenobiotics and synthesis of fatty acids. We find that only a small proportion of genes in these families are one-to-one orthologs and that their history is shaped by massive duplication events. Of a total of 349 and 528 genes from C. elegans and P. pacificus, respectively, only 39 are one-to-one orthologs. Thus, frequent amplifications and losses are a widespread phenomenon in nematode lineages. We also report variation in birth and death rates depending on gene families and nematode lineages. Finally, we discuss the consequence of the near absence of one-to-one orthology in related organisms for the application of the homology concept to protein-coding genes in the era of whole-genome sequencing data.

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DHS-21, a dicarbonyl/l -xylulose reductase (DCXR) ortholog, regulates longevity and reproduction in Caenorhabditis elegans

Cited by 10 publications

References 17 publications

Active transcriptomic and proteomic reprogramming in the C. elegans nucleotide excision repair mutant xpa-1

Active transcriptomic and proteomic reprogramming in the C. elegans nucleotide excision repair mutant xpa-1

Single-cell and bulk transcriptional profiling of mouse ovaries reveals novel genes and pathways associated with DNA damage response in oocytes

The Same or Not the Same: Lineage-Specific Gene Expansions and Homology Relationships in Multigene Families in Nematodes

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