Entrainment memories: What does stable mean?

Diurnal environmental factors (zeitgebers) set the circadian clock in an antagonistic way: The body clock is tuned forward in the morning, while the same factor late in the day puts the body clock back to a later time-point: Morning light, for example, reduces the clock-effective light-reception (zeitnehmer2 ) by shifting the expression of the circadian, light-processing, molecular machinery more into the late, light-less night. Evening light does the same by a backward-shift, respectively. The balance between these daily back and forth adaptations results in a synchronization of the organismic timing with its environment. Those traditional models are challenged in this study. Using Neurospora as a model, I will explore how the entrainment process follows diverging trajectories depending on zeitgeber structure and strength, and the kind of transition between different entraining situations. The diverging routes of entrainment, systematically becoming earlier and earlier or later and later until eventually settling in distinct entrained phases, point out the existence of a long-range "memory" component. The view of entrainment as a non-acute reaction is very well confirmed in feedback loops, limit cycles, phase-response curves, and so forth. However, the presented findings enhance an extension of those concepts: The processing of zeitgebers by oscillating zeitnehmer modules resulting in a certain temporal inner structuring is not fully established within one repetition along a unique reaction norm. I hypothesize that the long-range, multi-cycle component in entraining requires a third parameter of description additional to current internal phase and zeitgeber condition, which originates from the differential of the two or more consecutive periodic situations. I hypothesize that this differential is represented by a gradient of Gibbs free energy of the entrainment pathways. Low points of free energy identify stable phases of entrainment. The fundamentality of Gibbs energy puts entrainment up for discussion not only as a timer but as an important kind of homeostasis.

A peptide chain release factor 2 affects the stability of UGA-containing transcripts in Arabidopsis chloroplasts.

Positional cloning of the hcf109 (high chlorophyll fluorescence) mutation in Arabidopsis has identified a nucleus-encoded, plastid-localized release factor 2-like protein, AtprfB, indicating that the processes of translational termination in chloroplasts resemble those of eubacteria. Control of atprfB expression by light and tissues is connected to chloroplast development. A point mutation at the last nucleotide of the second intron causes a new splice site farther downstream, resulting in a deletion of seven amino acid residues in the N-terminal region of the Hcf109 protein. The mutation causes decreased stability of UGA-containing mRNAs. Our data suggest that transcripts with UGA stop codons are terminated exclusively by AtprfB in chloroplasts and that AtprfB is involved in the regulation of both mRNA stability and protein synthesis. Furthermore, sequence data reveal a +1 frameshift at an internal in-frame TGA stop codon in the progenitor prfB gene of cyanobacteria. The expression pattern and functions of atprfB could reflect evolutionary driving forces toward the conservation of TGA stop codons exclusively in plastid genomes of land plants.