Code breaking: The RNAPII modification code in pluripotency

Comment on: Brookes E, et al. Cell Stem Cell 2012; 10:157-70.     

Plant development: multiple strategies for breaking seed dormancy

Plant seeds will not germinate when in a dormant state. What then are the factors controlling dormancy? A recent study has uncovered two basic-helix-loop-helix proteins which repress germination and are critical for maintaining dormancy. The combined action of light and cold synergistically alleviates activity of these repressors thus stimulating germination.     

Aminoacyl-tRNA synthetases: potential markers of genetic code development

Aminoacylation of tRNAs, catalyzed by 20 aminoacyl-tRNA synthetases, is responsible for establishing the genetic code. The enzymes are divided into two classes on the basis of the architectures of their active sites. Members of the two classes also differ in that they bind opposite sides of the tRNA acceptor stem. Importantly, specific pairs of synthetases--one from each class--can be docked simultaneously onto the acceptor stem. This article relates these specific pairings to the organization of the table of codons that defines the universal genetic code.     

Language development.

Recent research suggests that our ability to learn language is innate, but not necessarily domain-specific. That is, language development appears to be based on a relatively plastic mix of neural systems that also serve other cognitive and perceptual functions. Evidence in support of this conclusion includes neural network simulations of language learning, event-related brain potential studies of normal language development, and studies of language development in several clinical populations of subjects suffering focal brain injury, specific language impairment, and contrasting forms of mental retardation.     

Genetic code development by stop codon takeover

A novel theoretical consideration of the origin and evolution of the genetic code is presented. Code development is viewed from the perspective of simultaneously evolving codons, anticodons and amino acids. Early code structure was determined primarily by thermodynamic stability considerations, requiring simplicity in primordial codes. More advanced coding stages could arise as biological systems became more complex and precise in their replication. To be consistent with these ideas, a model is described in which codons become permanently associated with amino acids only when a codon-anticodon pairing is strong enough to permit rapid translation. Hence all codons are essentially chain-termination or "stop" codons until tRNA adaptors evolve having the ability to bind tightly to them. This view, which draws support from several lines of evidence, differs from the prevalent thinking on code evolution which holds that codons specifying newer amino acids were derived from codons encoding older amino acids.     

Cadherin function: breaking the barrier

Three desmoglein isoforms collaborate with desmocollins to build the adhesive core of desmosomes. A recent study has shown that altering the ratio of desmoglein isoforms influences epidermal barrier function, suggesting distinct roles for these cadherins that extend beyond adhesion.     

Symmetry breaking and convergent extension in early chordate development

The initiation of axis, polarity, cell differentiation, and gastrulation in the very early chordate development is due to the breaking of radial symmetry. It is believed that this occurs by an external signal. We suggest instead spontaneous symmetry breaking through the agency of the Turing-Child field. Increased size or decreased diffusivity, both brought about by mitotic activity, cause the spontaneous loss of stability of the homogeneous state and the evolution of the metabolic pattern during development. The polar metabolic pattern is the cause of polar gene expression, polar morphogenesis (gastrulation), and polar mitotic activity. The Turing-Child theory explains not only the spontaneous formation of the invagination in gastrulation but also the coherent cell movement observed in convergence and extension during gastrulation and neurulation. The theory is demonstrated with respect to experimental observations on the early development of fish, amphibian, and the chick. The theory can explain a multitude of experimental details. For example, it explains the splayed polar progression of reduction in the fish blastoderm. Reduction starts on that side of the blastoderm margin, which will initiate invagination several hours later. It progresses toward the blastoderm center and somewhat laterally from this future "dorsal lip". This is precisely as predicted by a Turing-Child system in a circle. And for a fish like zebrafish with a blastoderm that is slightly oval, reduction is observed to progress along the long axis of the ellipse, which is what Turing-Child theory predicts. In general the shape and the chemical nature of the experimental patterns are the same as predicted by the Turing couple (cAMP, ATP). Embryological polarity and convergent extension are based on polar eigenfunction and saddle-shaped eigenfunction, respectively.     

Cytokinesis: breaking the ties that bind

It has been unclear how cells complete cell division and resolve membrane connections to bring about cell separation. Recent work has shown that targeted secretion to the midbody is required to complete cell division.     

Making and breaking the innervation of the ear: neurotrophic support during ear development and its clinical implications

Analyses of single and double mutants of members of the neurotrophin family and their receptors are reviewed. These data demonstrate that the two neurotrophins, brain-derived neurotrophic factor (BDNF) and neurotrophin 3 (NT-3), and their high-affinity receptors trkB and trkC, are the sole support for the developing afferent innervation of the ear. Neurotrophins are first expressed in the otocyst around the time afferent sensory neurons become postmitotic. They are crucial for the survival of certain topologically distinct populations of sensory neurons. BDNF supports all sensory neurons to the semicircular canals, most sensory neurons to the saccule and utricle, and many sensory neurons to the apex and middle turn of the cochlea. In contrast, NT-3 supports few sensory neurons to the utricle and saccule, all sensory neurons to the basal turn of the cochlea and most sensory neurons to the middle and apical turn. Some topologically restricted effects reflect the pattern of neurotrophin distribution as revealed by in situ hybridization (e.g., loss of all innervation to the semicircular canal sensory epithelia in BDNF or trkB mutants). However, other topologically restricted effects cannot be explained on the basis of current knowledge of neurotrophin or neurotrophin receptor distribution. Data on mutants also support the notion that BDNF may play a role in neonatal plastic reorganization of the pattern of innervation in the ear and possibly the brainstem. In contrast, data obtained thus far on the ability of neurotrophins to rescue adult sensory neuron after insults to cochlear hair cells are less compelling. The ear is a model system to test the interactions of the two neurotrophins, BDNF and NT-3, with their two high-affinity receptors, trkB and trkC.