Hox genes in the coordination of embryonic development. Model of hourglass in the description of vertebrate ontogenesis

The paper analyzes the role of HOX genes in the processes of embryonic development of vertebrates. Based on the analysis, it is concluded that HOX genes are the most important regulators of embryonic development. The HOX genes predominantly realize their influence through specific HOX proteins that have the ability to regulate the expression of target genes. The order of expression of the HOX genes, as a rule, obeys the rule of temporal and spatial colinearity. This mechanism determines the temporal and spatial course of tissue morphogenesis during embryonic development and tissue regeneration in organisms that have reached the stage of maturity. The process of embryo morphogenesis, determined by highly conserved HOX genes, explains the appearance of the phylotypic period - the stage of embryonic development of vertebrates, at which embryos of different classes of vertebrates have distinct morphological similarities.

The function of α-Catenin mechanosensing in tissue morphogenesis

Abstractα-catenin couples the cadherin-catenin complex to the actin cytoskeleton. The mechanosensitive α-catenin M region undergoes conformational changes upon application of force to recruit binding partners. Here, we took advantage to the tension landscape in the Drosophila embryo to define three different states of α-catenin mechanosensing in support of cell adhesion. Low, medium, and high tension contacts showed α-catenin M region-dependent low, medium, and high levels of Vinculin and Ajuba recruitment. In contrast, Afadin/Canoe acts in parallel to α-catenin at bicellular low and medium tension junctions, but requires an interaction with α-catenin for its tension-sensitive enrichment at high-tension tricellular junctions. Individual M region domains make complex contributions to cell adhesion through their impact on binding partner recruitment, and redundancies with the function of Afadin/Canoe. Our data argue that α-catenin and its interaction partners are part of a cooperative and partially redundant, mechanoresponsive network that supports AJs remodelling during morphogenesis.

Cell wall damage attenuates root hair patterning and tissue morphogenesis mediated by the receptor kinase STRUBBELIG

ABSTRACT Cell wall remodeling is essential for the control of growth and development as well as the regulation of stress responses. However, the underlying cell wall monitoring mechanisms remain poorly understood. Regulation of root hair fate and flower development in Arabidopsis thaliana requires signaling mediated by the atypical receptor kinase STRUBBELIG (SUB). Furthermore, SUB is involved in cell wall integrity signaling and regulates the cellular response to reduced levels of cellulose, a central component of the cell wall. Here, we show that continuous exposure to sub-lethal doses of the cellulose biosynthesis inhibitor isoxaben results in altered root hair patterning and floral morphogenesis. Genetically impairing cellulose biosynthesis also results in root hair patterning defects. We further show that isoxaben exerts its developmental effects through the attenuation of SUB signaling. Our evidence indicates that downregulation of SUB is a multi-step process and involves changes in SUB complex architecture at the plasma membrane, enhanced removal of SUB from the cell surface, and downregulation of SUB transcript levels. The results provide molecular insight into how the cell wall regulates cell fate and tissue morphogenesis.

Decoding Cell Death: From a Veritable Library of Babel to Vade Mecum?

Programmed cell death (PCD) is a requisite feature of development and homeostasis but can also be indicative of infections, injuries, and pathologies. In concordance with these heterogeneous contexts, an array of disparate effector responses occur downstream of cell death and its clearance—spanning tissue morphogenesis, homeostatic turnover, host defense, active dampening of inflammation, and tissue repair. This raises a fundamental question of how a single contextually appropriate response ensues after an event of PCD. To explore how complex inputs may together tailor the specificity of the resulting effector response, here we consider ( a) the varying contexts during which different cell death modalities are observed, ( b) the nature of the information that can be passed on by cell corpses, and ( c) the ways by which efferocyte populations synthesize signals from dying cells with those from the surrounding microenvironment.