Model for the formation of a microscopic Turing structure: The facetting of Pt(110) during catalytic oxidation of CO

A Monte Carlo simulation of the formation of regular facet patterns during catalytic CO oxidation on Pt(110) has been conducted. The simulation was based on the elementary steps of the surface reaction, the CO-induced 1×1⇄1×2 phase transition, and the enhancement of O2 adsorption at step sites. The model can reproduce the formation of sawtoothlike facet patterns with a spacing of ∼100 to 200 Å. The facets represent a Turing structure caused by the coupling of kinetic instabilities with the mass transport of Pt atoms

Formation of Turing structures in catalytic surface reactions: The facetting of Pt(110) in CO+O₂

The Pt(110) surface facets during the catalytic oxidation of CO, if reaction conditions are adjusted such that the CO‐induced 1×1⇄1×2 phase transition can take place simultaneously. A detailed low‐energy electron diffraction beam profile analysis revealed that regularly spaced (430) and (340) facets are formed with a lateral periodicity of ∼70 lattice units along the [11̄0] direction. This result, together with the observation that the facetted surface is only stable under reaction conditions, indicates a dissipative structure of the Turing type. Such structures, which are stationary but exhibit a periodic variation of the concentration variables in space, have so far almost exclusively been discussed theoretically. The interpretation of the facetted surface as a Turing structure could be confirmed by a Monte Carlo simulation based on the Langmuir Hinshelwood mechanism of catalytic CO oxidation and the CO‐induced 1×1⇄1×2 phase transition

Fate specification and tissue-specific cell cycle control of the <i>Caenorhabditis elegans</i> intestine

Coordination between cell fate specification and cell cycle control in multicellular organisms is essential to regulate cell numbers in tissues and organs during development, and its failure may lead to oncogenesis. In mammalian cells, as part of a general cell cycle checkpoint mechanism, the F-box protein β-transducin repeat-containing protein (β-TrCP) and the Skp1/Cul1/F-box complex control the periodic cell cycle fluctuations in abundance of the CDC25A and B phosphatases. Here, we find that the Caenorhabditis elegans β-TrCP orthologue LIN-23 regulates a progressive decline of CDC-25.1 abundance over several embryonic cell cycles and specifies cell number of one tissue, the embryonic intestine. The negative regulation of CDC-25.1 abundance by LIN-23 may be developmentally controlled because CDC-25.1 accumulates over time within the developing germline, where LIN-23 is also present. Concurrent with the destabilization of CDC-25.1, LIN-23 displays a spatially dynamic behavior in the embryo, periodically entering a nuclear compartment where CDC-25.1 is abundant