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Facial attractiveness is a complex human trait of great interest in both academia and industry. Literature on sociological and phenotypic factors associated with facial attractiveness is rich, but its genetic basis is poorly understood. In this paper, we conducted a genome-wide association study to discover genetic variants associated with facial attractiveness using 4,383 samples in the Wisconsin Longitudinal Study. We identified two genome-wide significant loci, highlighted a handful of candidate genes, and demonstrated enrichment for heritability in human tissues involved in reproduction and hormone synthesis. Additionally, facial attractiveness showed strong and negative genetic correlations with BMI in females and with blood lipids in males. Our analysis also suggested sex-specific selection pressure on variants associated with lower male attractiveness. These results revealed sex-specific genetic architecture of facial attractiveness and provided fundamental new insights into its genetic basis. [ABSTRACT FROM AUTHOR]

The roles of histone demethylation in the regulation of plant flowering, disease resistance, rhythmical response, and seed germination have been elucidated recently; however, how histone demethylation affects leaf senescence remains largely unclear. In this study, we exploited yeast one-hybrid (Y1H) to screen for the upstream regulators of NONYELLOWING1 (NYE1), and identified RELATIVE OF EARLY FLOWERING6 (REF6), a histone H3 lysine 27 tri-methylation (H3K27me3) demethylase, as a putative binding protein of NYE1 promoter. By in vivo and in vitro analyses, we demonstrated that REF6 directly binds to the motif CTCGYTY in NYE1/2 promoters through its zinc finger domain and positively regulates their expression. Loss-of-function of REF6 delayed chlorophyll (Chl) degradation, whereas overexpression of REF6 accelerated Chl degradation. Subsequently, we revealed that REF6 positively regulates the general senescence process by directly up-regulating ETHYLENE INSENSITIVE 2 (EIN2), ORESARA1 (ORE1), NAC-LIKE, ACTIVATED BY AP3/PI (NAP), PYRUVATE ORTHOPHOSPHATE DIKINASE (PPDK), PHYTOALEXIN DEFICIENT 4 (PAD4), LIPOXYGENASE 1 (LOX1), NAC DOMAIN CONTAINING PROTEIN 3 (AtNAC3), and NAC TRANSCRIPTION FACTOR-LIKE 9 (NTL9), the key regulatory and functional genes predominantly involved in the regulation of developmental leaf senescence. Importantly, loss-of-function of REF6 increased H3K27me3 levels at all the target Senescence associated genes (SAGs). We therefore conclusively demonstrate that H3K27me3 methylation represents an epigenetic mechanism prohibiting the premature transcriptional activation of key developmentally up-regulated senescence regulatory as well as functional genes in Arabidopsis. [ABSTRACT FROM AUTHOR]

Plant roots are constantly exposed to a variety of abiotic stresses, and high salinity is one of the major limiting conditions that impose constraints on plant growth. In this study, we describe that OsMADS25 is required for the root growth as well as salinity tolerance, via maintaining ROS homeostasis in rice (Oryza sativa). Overexpression of OsMADS25 remarkably enhanced the primary root (PR) length and lateral root (LR) density, whereas RNAi silence of this gene reduced PR elongation significantly, with altered ROS accumulation in the root tip. Transcriptional activation assays indicated that OsMADS25 activates OsGST4 (glutathione S–transferase) expression directly by binding to its promoter. Meanwhile, osgst4 mutant exhibited repressed growth and high sensitivity to salinity and oxidative stress, and recombinant OsGST4 protein was found to have ROS–scavenging activity in vitro. Expectedly, overexpression of OsMADS25 significantly enhanced the tolerance to salinity and oxidative stress in rice plants, with the elevated activity of antioxidant enzymes, increased accumulation of osmoprotective solute proline and reduced frequency of open stoma. Furthermore, OsMADS25 specifically activated the transcription of OsP5CR, a key component of proline biosynthesis, by binding to its promoter. Interestingly, overexpression of OsMADS25 raised the root sensitivity to exogenous ABA, and the expression of ABA–dependent stress–responsive genes was elevated greatly in overexpression plants under salinity stress. In addition, OsMADS25 seemed to promote auxin signaling by activating OsYUC4 transcription. Taken together, our findings reveal that OsMADS25 might be an important transcriptional regulator that regulates the root growth and confers salinity tolerance in rice via the ABA–mediated regulatory pathway and ROS scavenging. [ABSTRACT FROM AUTHOR]

Misfolded proteins challenge the ability of cells to maintain protein homeostasis and can accumulate into toxic protein aggregates. As a consequence, cells have adopted a number of protein quality control pathways to prevent protein aggregation, promote protein folding, and target terminally misfolded proteins for degradation. In this study, we employed a thermosensitive allele of the yeast Guk1 guanylate kinase as a model misfolded protein to investigate degradative protein quality control pathways. We performed a flow cytometry based screen to identify factors that promote proteasomal degradation of proteins misfolded as the result of missense mutations. In addition to the E3 ubiquitin ligase Ubr1, we identified the prefoldin chaperone subunit Gim3 as an important quality control factor. Whereas the absence of GIM3 did not impair proteasomal function or the ubiquitination of the model substrate, it led to the accumulation of the poorly soluble model substrate in cellular inclusions that was accompanied by delayed degradation. We found that Gim3 interacted with the Guk1 mutant allele and propose that prefoldin promotes the degradation of the unstable model substrate by maintaining the solubility of the misfolded protein. We also demonstrated that in addition to the Guk1 mutant, prefoldin can stabilize other misfolded cytosolic proteins containing missense mutations. [ABSTRACT FROM AUTHOR]