One hundred DDB1 (damaged DNA binding protein-1)-binding WD40-repeat domain (DWD) family genes were identified in the S. lycopersicum genome. The DWD genes encode proteins presumably functioning as the substrate recognition subunits of the cullin4-ring ubiquitin E3 ligase complex. These findings provide candidate genes and a research platform for further gene functionality and molecular breeding study. A subclass of DDB1 (damaged DNA binding protein-1)-binding WD40-repeat domain (DWD) family proteins has been demonstrated to function as the substrate recognition subunits of the cullin4-ring ubiquitin E3 ligase complex. However, little information is available about the cognate subfamily genes in tomato (S. lycopersicum). In this study, based on the recently released tomato genome sequences, 100 tomato genes encoding DWD proteins that potentially interact with DDB1 were identified and characterized, including analyses of the detailed annotations, chromosome locations and compositions of conserved amino acid domains. In addition, a phylogenetic tree, which comprises of three main groups, of the subfamily genes was constructed. The physical interaction between tomato DDB1 and 14 representative DWD proteins was determined by yeast two-hybrid and co-immunoprecipitation assays. The subcellular localization of these 14 representative DWD proteins was determined. Six of them were localized in both nucleus and cytoplasm, seven proteins exclusively in cytoplasm, and one protein either in nucleus and cytoplasm, or exclusively in cytoplasm. Comparative genomic analysis demonstrated that the expansion of these subfamily members in tomato predominantly resulted from two whole-genome triplication events in the evolution history.

Download full-text PDF

Source
http://dx.doi.org/10.1007/s00425-015-2258-8DOI Listing

Publication Analysis

Top Keywords

ddb1 damaged
12
damaged dna
12
dna binding
12
binding protein-1-binding
12
protein-1-binding wd40-repeat
12
dwd proteins
12
wd40-repeat domain
8
domain dwd
8
dwd family
8
substrate recognition
8

Similar Publications

Lysosomes are the major cellular organelles responsible for nutrient recycling and degradation of cellular material. Maintenance of lysosomal integrity is essential for cellular homeostasis and lysosomal membrane permeabilization (LMP) sensitizes toward cell death. Damaged lysosomes are repaired or degraded via lysophagy, during which glycans, exposed on ruptured lysosomal membranes, are recognized by galectins leading to K48- and K63-linked poly-ubiquitination (poly-Ub) of lysosomal proteins followed by recruitment of the macroautophagic/autophagic machinery and degradation.

View Article and Find Full Text PDF

Interaction of DDB1 with NBS1 in a DNA Damage Checkpoint Pathway.

Int J Mol Sci

December 2024

Department of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Seoul 06351, Republic of Korea.

Various DNA damage checkpoint control mechanisms in eukaryotic cells help maintain genomic integrity. Among these, NBS1, a key component of the MRE11-RAD50-NBS1 (MRN) complex, is an essential protein involved in the DNA damage response (DDR). In this study, we discovered that DNA damage-binding protein 1 (DDB1) interacts with NBS1.

View Article and Find Full Text PDF

EIF4A3-Induced Circular RNA CircDdb1 Promotes Muscle Atrophy through Encoding a Novel Protein CircDdb1-867aa.

Adv Sci (Weinh)

December 2024

Cardiac Regeneration and Ageing Lab, Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong) and School of Life Sciences, Shanghai University, Nantong, 226011, China.

Article Synopsis
  • Researchers have identified a specific circular RNA, circDdb1, that plays a significant role in causing skeletal muscle atrophy, which is often linked to aging and various diseases.
  • CircDdb1 levels are significantly increased during muscle atrophy, and adding it artificially leads to more atrophy, whereas its inhibition can prevent muscle loss caused by different factors.
  • The study also finds that circDdb1 regulates protein translation via its interaction with eukaryotic elongation factor 2 (eEF2) and suggests that targeting circDdb1 could serve as a new therapeutic approach to combat muscle atrophy.
View Article and Find Full Text PDF

Effects of Zinc Phthalocyanine Photodynamic Therapy on Vital Structures and Processes in Hela Cells.

Int J Mol Sci

October 2024

Department of Medical Biophysics, Faculty of Medicine and Dentistry, Palacky University, 77900 Olomouc, Czech Republic.

This work presents results on the efficiency of newly designed zinc phthalocyanine-mediated photodynamic therapy of both tumoral and nontumoral cell models using the MTT assay. Further detailed examinations of mechanistic and cell biological effects were focused on the HELA cervical cancer cell model. Here, ROS production, changes in the mitochondrial membrane potential, the determination of genotoxicity, and protein changes determined by capillary chromatography and tandem mass spectrometry with ESI were analyzed.

View Article and Find Full Text PDF

USP14 inhibition promotes DNA damage repair and represses ovarian granulosa cell senescence in premature ovarian insufficiency.

J Transl Med

September 2024

Center for Reproductive Medicine, Department of Gynecology and Obstetrics, Nanfang Hospital, Southern Medical University, No. 1838 Guangzhou Northern Road, Guangzhou, Guangdong, 510515, China.

Background: Premature ovarian insufficiency (POI) is a condition characterized by a substantial decline or loss of ovarian function in women before the age of 40. However, the pathogenesis of POI remains to be further elucidated, and specific targeted drugs which could delay or reverse ovarian reserve decline are urgently needed. Abnormal DNA damage repair (DDR) and cell senescence in granulosa cells are pathogenic mechanisms of POI.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!