8 research outputs found
Phylogenetic analysis of the CDGSH iron-sulfur binding domain reveals its ancient origin
The iron-sulfur (2Fe-2S) binding motif CDGSH appears in many important plant and animal proteins that regulate iron and reactive oxygen metabolism. In human it is found in CISD1-3 proteins involved in diabetes, obesity, cancer, aging, cardiovascular disease and neurodegeneration. Despite the important biological role of the CDGSH domain, its origin, evolution and diversification, are largely unknown. Here, we report that: (1) the CDGSH domain appeared early in evolution, perhaps linked to the heavy use of iron-sulfur driven metabolism by early organisms; (2) a CISD3-like protein with two CDGSH domains on the same polypeptide appears to represent the ancient archetype of CDGSH proteins; (3) the origin of the human CISD3 protein is linked to the mitochondrial endosymbiotic event; (4) the CISD1/2 type proteins that contain only one CDGSH domain, but function as homodimers, originated after the divergence of bacteria and archaea/eukaryotes from their common ancestor; and (5) the human CISD1 and CISD2 proteins diverged about 650–720 million years ago, and CISD3 and CISD1/2 share their descent from an ancestral CISD about 1–1.1 billion years ago. Our findings reveal that the CDGSH domain is ancient in its origin and shed light on the complex evolutionary path of modern CDGSH proteins
Oxidative stress, growth inhibition, and DNA damage in earthworms induced by the combined pollution of typical neonicotinoid insecticides and heavy metals
Comparative studies on tolerance of rice genotypes differing in their tolerance to moderate salt stress
The cisd gene family regulates physiological germline apoptosis through ced-13 and the canonical cell death pathway in Caenorhabditis elegans
This article examines how the disruption of the cisd-1 gene function, using RNA interference (RNAi), or mutant alleles [cisd-1(tm4993) deletion mutant, cisd-1(pnIs27) insertion mutant] led to germline abnormalities including an increase in the number of cell corpses and distal tip cell migration defects