The Genomics of Oryza Species Provides Insights into Rice Domestication and Heterosis

Here, we review recent progress in genetic and genomic studies of the diversity of Oryza species. In recent years, unlocking the genetic diversity of Oryza species has provided insights into the genomics of rice domestication, heterosis, and complex traits. Genome sequencing and analysis of numerous wild rice (Oryza rufipogon) and Asian cultivated rice (Oryza sativa) accessions have enabled the identification of genome-wide signatures of rice domestication and the unlocking of the origin of Asian cultivated rice. Moreover, similar studies on genome variations of African rice (Oryza glaberrima) cultivars and their closely related wild progenitor Oryza barthii accessions have provided strong evidence to support a theory of independent domestication in African rice. Integrated genomic approaches have efficiently investigated many heterotic loci in hybrid rice underlying yield heterosis advantages and revealed the genomic architecture of rice heterosis. We conclude that in-depth unlocking of genetic variations among Oryza species will further enhance rice breeding

Mitochondrial Effects of PGC-1alpha Silencing in MPP+ Treated Human SH-SY5Y Neuroblastoma Cells

The dopaminergic neuron degeneration and loss that occurs in Parkinson’s disease (PD) has been tightly linked to mitochondrial dysfunction. Although the aged-related cause of the mitochondrial defect observed in PD patients remains unclear, nuclear genes are of potential importance to mitochondrial function. Human peroxisome proliferator-activated receptor γ coactivator-1alpha (PGC-1α) is a multi-functional transcription factor that tightly regulates mitochondrial biogenesis and oxidative capacity. The goal of the present study was to explore the potential pathogenic effects of interference by the PGC-1α gene on N-methyl-4-phenylpyridinium ion (MPP+)-induced SH-SY5Y cells. We utilized RNA interference (RNAi) technology to probe the pathogenic consequences of inhibiting PGC-1α in the SH-SY5Y cell line. Remarkably, a reduction in PGC-1α resulted in the reduction of mitochondrial membrane potential, intracellular ATP content and intracellular H2O2 generation, leading to the translocation of cytochrome c (cyt c) to the cytoplasm in the MPP+-induced PD cell model. The expression of related proteins in the signaling pathway (e.g., estrogen-related receptor α (ERRα), nuclear respiratory factor 1 (NRF-1), NRF-2 and Peroxisome proliferator-activated receptor γ (PPARγ)) also decreased. Our finding indicates that small interfering RNA (siRNA) interference targeting the PGC-1α gene could inhibit the function of mitochondria in several capacities and that the PGC-1α gene may modulate mitochondrial function by regulating the expression of ERRα, NRF-1, NRF-2 and PPARγ. Thus, PGC-1α can be considered a potential therapeutic target for PD