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In studying holistic face processing across the life-span there are only few attempts to separate face-specific from general aging effects. Here we used the complete design of the composite paradigm (Cheung et al., 2008) with faces and novel non-face control objects (watches) to investigate composite effects in young (18-32 years) and older adults (63-78 years). We included cueing conditions to alert using a narrow or a wide attentional focus when comparing the composite objects, and used brief and relaxed exposure durations for stimulus presentation. Young adults showed large composite effects for faces, but none for watches. In contrast, older adults showed strong composite effects for faces and watches, albeit the effects were larger for faces. Moreover, composite effects for faces were larger for the wide attentional focus in both age groups, while the composite effects for watches of older adults were alike for both cueing conditions. Older adults showed low accuracy at the same levels for both types of stimuli when attended and non-attended halves were incongruent. Increasing presentation times improved performance strongly for congruent but not for incongruent composite objects. These findings suggest that the composite effects of older adults reflect substantial decline in the ability to control irrelevant stimuli, which takes effect both in non-face objects and in faces. In young adults, highly efficient attentional control mostly precludes interference of irrelevant features in novel objects, thus their composite effects reflect holistic integration specific for faces or objects of expertise. [ABSTRACT FROM AUTHOR]

In response to oxidative stress, cells decide whether to mount a survival or cell death response. The conserved cyclin C and its kinase partner Cdk8 play a key role in this decision. Both are members of the Cdk8 kinase module, which, with Med12 and Med13, associate with the core mediator complex of RNA polymerase II. In Saccharomyces cerevisiae , oxidative stress triggers Med13 destruction, which thereafter releases cyclin C into the cytoplasm. Cytoplasmic cyclin C associates with mitochondria, where it induces hyperfragmentation and regulated cell death. In this report, we show that residues 742-844 of Med13's 600-amino acid intrinsic disordered region (IDR) both directs cyclin C-Cdk8 association and serves as the degron that mediates ubiquitin ligase SCF Grr1 -dependent destruction of Med13 following oxidative stress. Here, cyclin C-Cdk8 phosphorylation of Med13 most likely primes the phosphodegron for destruction. Next, pro-oxidant stimulation of the cell wall integrity pathway MAP kinase Slt2 initially phosphorylates cyclin C to trigger its release from Med13. Thereafter, Med13 itself is modified by Slt2 to stimulate SCF Grr1 -mediated destruction. Taken together, these results support a model in which this IDR of Med13 plays a key role in controlling a molecular switch that dictates cell fate following exposure to adverse environments., (© 2018 Stieg et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).)