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Computational morphodynamics has provided great insights into the highly dynamic process of plant development. This is because it combines live imaging to observe development as it happens, image processing to extract data, and computational modelling to test hypotheses against quantitative information.
Unlike somatic cells, stem cells persist throughout life, which may increase their risk of accumulating DNA damage. recent studies indicate that stem cells use different mechanisms (such as the error-prone non-homologous end joining pathway) from somatic cells to maintain genomic integrity, which could have deleterious consequences for their long-term function.
Mesenchymal stem cells (MSCs) are multipotent progenitors derived from tissue stroma that differentiate into adipocytes, chondrocytes and osteoblasts when expandedin vitro. Although the properties of the in vitro-expanded progeny are well defined, the in vivobiology of MSCs is only just beginning to be elucidated.
Single-cell measurements and lineage-tracing experiments are revealing that cell-to-cell variability is often the result of deterministic processes, despite the existence of intrinsic noise in molecular networks. As this determinism usually represents uncharacterized molecular regulatory mechanisms, cell-to-cell variability should be studied as a discipline of molecular cell biology.
The mechanisms regulating the import of proteins into peroxisomes share surprising similarities with those controlling the degradation of proteins at the endoplasmic reticulum. These unexpected parallels may result from the common molecular machinery used to tag substrates and drive their removal from the membrane.
Aminoacyl tRNA synthetases (aaRSs) have progressively added domains and motifs that have no connection to aminoacylation. These additions equip aaRSs with new functions and correlate with the appearance of new biological processes (such as a circulatory system) during the course of evolution.
Recent studies suggest that the spindle matrix provides a conserved strategy to coordinate the segregation of genetic material and the partitioning of other cellular contents in open, partially open and closed mitosis.
Current descriptions of eukaryotic chemotaxis focus on how extracellular signals (chemoattractants) cause new pseudopods to form. However, reinterpretation of recent data suggests a 'pseudopod-centred' explanation, whereby most pseudopods form without exogenous signals and chemoattractants only bias the position and rate of pseudopod growth.
GW182 proteins are key components of microRNA silencing complexes in animals, although their precise molecular function has been poorly understood. Recent findings indicate that they promote gene silencing by interfering with cytoplasmic poly(A)-binding protein 1 (PABPC1) function during translation and mRNA stabilization — a mode of action similar to that of PABP-interacting protein 2 (PAIP2).
Neurodegenerative diseases are associated with the accumulation of intracellular or extracellular protein aggregates that form because of protein misfolding. These aggregates are capable of crossing cellular membranes and can thereby directly contribute to the propagation of neurodegenerative disease pathogenesis, which might spread in a 'prion-like' manner.
A contractile ring of actin filaments and myosin II generates the force that constricts the cleavage furrow of animal cells, leading to cytokinesis. Studies in fission yeast have increased our understanding of the mechanisms of cytokinesis, which are likely to be conserved in other organisms.
The cytoskeleton is a dynamic fibrous network that has essential roles in the generation and regulation of cell architecture. It has also evolved as a scaffold that anchors various biochemical pathways, and might participate in the spatial organization and regulation of translation.
Most kinesins move processively along microtubules using energy derived from ATP hydrolysis. Almost all of the intermediate structures of this ATPase reaction cycle have been solved for the monomeric kinesin 3 family motor KIF1A. These structures suggest that kinesins might move by a common mechanism.
During cell division, the asymmetric localization of epigenetic marks and kinetochore proteins might lead to the differential recognition of sister chromatids and the biased segregation of DNA strands to daughter cells. This might ultimately result in the acquisition of distinct cell fates after mitosis.
The reconstitution of biological processes from purified components is a powerful approach to understanding the principles that govern cellular organization. The recent development of new experimental techniques is enabling the reconstitution of increasingly complex cellular systems.
The growth of microtubules is accompanied by large fluctuations in rates and abrupt transitions between phases of growth and shrinkage. The authors propose that fluctuations in the length of the GTP–tubulin cap at the microtubule end could be the main source of variation.
In interphase, chromosomes are associated with proteins and RNAs that participate in many metabolic processes. During mitosis, these components might inhibit chromosome segregation or reduce its fidelity. The author proposes the existence of a molecular mechanism that eliminates unwanted components from mitotic chromosomes.
Compositionally and functionally distinct RNA granules are found in the cytoplasm of somatic and germ cells. The components of most RNA granules are in a dynamic equilibrium, thereby allowing rapid shifts between the translation, storage and decay of RNAs.
Protein sumoylation affects many biological processes, but it was not previously thought to target proteins for degradation. Recent findings unravel a new role for small ubiquitin-like modifier (SUMO) as a signal for the recruitment of ubiquitin ligases, which leads to protein ubiquitylation and degradation.
Guanine nucleotide-binding (G) proteins are regulated by GTPase-activating proteins and guanine nucleotide-exchange factors. Another class of G proteins is emerging that are regulated by homodimerization. The authors propose that juxtaposition of the G domains of two monomers across the GTP-binding sites activates the biological function of these proteins and the GTPase reaction.