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The contrast and resolution of images obtained with optical microscopes can be improved by deconvolution and computational fusion of multiple views of the same sample, but these methods are computationally expensive for large datasets. Here we describe theoretical and practical advances in algorithm and software design that result in image processing times that are tenfold to several thousand fold faster than with previous methods. First, we show that an ‘unmatched back projector’ accelerates deconvolution relative to the classic Richardson–Lucy algorithm by at least tenfold. Second, three-dimensional image-based registration with a graphics processing unit enhances processing speed 10- to 100-fold over CPU processing. Third, deep learning can provide further acceleration, particularly for deconvolution with spatially varying point spread functions. We illustrate our methods from the subcellular to millimeter spatial scale on diverse samples, including single cells, embryos and cleared tissue. Finally, we show performance enhancement on recently developed microscopes that have improved spatial resolution, including dual-view cleared-tissue light-sheet microscopes and reflective lattice light-sheet microscopes. Microscopy datasets are processed orders-of-magnitude faster with improved algorithms and deep learning.

The Great Salt Lake comprises two high salinity arms, the North at 34% salinity, and the larger South at 16%. The biodegradation of gasoline range alkanes, cycloalkanes, aromatics, alkenes and cycloalkenes was extensive in samples from both arms, although slower than in fresh- and sea-water. Less volatile hydrocarbons in weathered crude oil were degraded less extensively, and again more slowly than in sea or fresh-water. The substrates subject to degradation are substantially more diverse than has previously been reported, and indicate that biodegradation will likely be the eventual fate of any petroleum hydrocarbons that enter the lake and do not evaporate. The biodegradation is, however, much slower than in other environments, and we discuss whether it might be increased to meet anthropogenic pollution, perhaps by nutrient supplementation with organic nitrogen.

Key Points Genomic sequence analysis is revealing the presence of duplicated genes in all sequenced organisms. Gene duplicates can arise through tandem, segmental or global duplication events. In instances in which complete regulatory sequences are duplicated in concert with coding sequences, the duplicates will have highly redundant functions. Classical models predict that the loss of one redundant duplicate will be the most likely evolutionary outcome, whereas the retention of two duplicates — because one takes on a new role — should happen far more rarely. Sub-functionalization models might help to explain the surprising number of ancient duplicates that are retained in genomes. If each duplicate loses a complementary sub-function then both must be retained to recapitulate the complete function of the single ancestral gene. Sub-functionalization relies on the inherent multifunctionality of genes, this is often provided by modular enhancers that direct specific components of gene expression patterns. The duplication–degeneration–complementation (DDC) model integrates gene-level sub-functionalization with population-level evolutionary processes. Species in which whole-genome duplication events have occurred, such as zebrafish and Arabidopsis , are providing useful systems to explore potential instances of degenerative complementation. Sophisticated sequence analysis approaches are starting to open up the possibility of recognizing candidate cases of sub-functionalization in silico . Many genes are members of large families that have arisen during evolution through gene duplication events. Our increasing understanding of gene organization at the scale of whole genomes is revealing further evidence for the extensive retention of genes that arise during duplication events of various types. Duplication is thought to be an important means of providing a substrate on which evolution can work. An understanding of gene duplication and its resolution is crucial for revealing mechanisms of genetic redundancy. Here, we consider both the theoretical framework and the experimental evidence to explain the preservation of duplicated genes.

Coordination of cell proliferation and migration is fundamental for life, and its dysregulation has catastrophic consequences, such as cancer. How cell cycle progression affects migration, and vice versa, remains largely unknown. We address these questions by combining in silico modelling and in vivo experimentation in the zebrafish trunk neural crest (TNC). TNC migrate collectively, forming chains with a leader cell directing the movement of trailing followers. We show that the acquisition of migratory identity is autonomously controlled by Notch signalling in TNC. High Notch activity defines leaders, while low Notch determines followers. Moreover, cell cycle progression is required for TNC migration and is regulated by Notch. Cells with low Notch activity stay longer in G 1 and become followers, while leaders with high Notch activity quickly undergo G 1 /S transition and remain in S-phase longer. In conclusion, TNC migratory identities are defined through the interaction of Notch signalling and cell cycle progression.

The Actinopterygii (ray-finned fishes) is the largest and most diverse vertebrate group, but little is agreed about the timing of its early evolution. Estimates using mitochondrial genomic data suggest that the major actinopterygian clades are much older than divergence dates implied by fossils. Here, the timing of the evolutionary origins of these clades is reinvestigated using morphological, and nuclear and mitochondrial genetic data. Results indicate that existing fossil-based estimates of the age of the crown-group Neopterygii, including the teleosts, Lepisosteus (gar) and Amia (bowfin), are at least 40 Myr too young. We present new palaeontological evidence that the neopterygian crown radiation is a Palaeozoic event, and demonstrate that conflicts between molecular and morphological data for the age of the Neopterygii result, in part, from missing fossil data. Although our molecular data also provide an older age estimate for the teleost crown, this range extension remains unsupported by the fossil evidence. Nuclear data from all relevant clades are used to demonstrate that the actinopterygian whole-genome duplication event is teleost-specific. While the date estimate of this event overlaps the probable range of the teleost stem group, a correlation between the genome duplication and the large-scale pattern of actinopterygian phylogeny remains elusive.

Cancer stem cells are recognized as the most critical cancer cells. They are responsible for cancer progression, the development of metastasis, and treatment failures. There are a number of well-studied surface proteins and enzymatic processes that can be used to isolate cancer stem cells from the bulk of the other cancer cells. The role of cancer stems cells in premalignant lesions of the oral cancer is poorly understood but slowly evolving. Novel therapies are being developed to more effectively eradicate cancer stem cells and improve patient outcomes. Efforts to improve our understanding of this important subpopulation of cancer cells is vital in directing further studies to advance our ability to prevent patients from developing oral cancer and to providing more effective treatment for those that do.

The control of organ size and position relies, at least in part, upon appropriate regulation of the signals that specify organ progenitor fields. Pancreatic cell fates are specified by retinoic acid (RA), and proper size and localization of the pancreatic field are dependent on tight control of RA signaling. Here we show that the RA-degrading Cyp26 enzymes play a critical role in defining the normal anterior limit of the pancreatic field. Disruption of Cyp26 function causes a dramatic expansion of pancreatic cell types toward the anterior of the embryo. The cyp26a1 gene is expressed in the anterior trunk endoderm at developmental stages when RA is signaling to specify pancreas, and analysis of cyp26a1/giraffe (gir) mutant zebrafish embryos confirms that cyp26a1 plays the primary role in setting the anterior limit of the pancreas. Analysis of the gir mutants further reveals that cyp26b1 and cyp26c1 function redundantly to partially compensate for loss of Cyp26a1 function. We used cell transplantation to determine that Cyp26a1 functions directly in endoderm to modulate RA signaling and limit the pancreatic field. Taken together with our finding that endodermal expression of cyp26 genes is subject to positive regulation by RA, our data reveal a feedback loop within the endoderm. Such feedback can maintain consistent levels of RA signaling, despite environmental fluctuations in RA concentration, thus ensuring a consistent size and location of the pancreatic field.

The mechanosensory lateral line system of aquatic vertebrates comprises a superficial network of distributed sensory organs, the neuromasts, which are arranged over the head and trunk and innervated by lateral line nerves to allow detection of changes in water flow and pressure. While the well-studied zebrafish posterior lateral line has emerged as a powerful model to study collective cell migration, far less is known about development of the anterior lateral line, which produces the supraorbital and infraorbital lines around the eye, as well as mandibular and opercular lines over the jaw and cheek. Here we show that normal development of the zebrafish anterior lateral line system from cranial placodes is dependent on another vertebrate-specific cell type, the cranial neural crest. We find that cranial neural crest and anterior lateral lines develop in close proximity, with absence of neural crest cells leading to major disruptions in the overlying anterior lateral line system. Specifically, in the absence of neural crest neither supraorbital nor infraorbital lateral lines fully extend, such that the most anterior cranial regions remain devoid of neuromasts, while supernumerary ectopic neuromasts form in the posterior supraorbital region. Both neural crest and cranial placodes contribute neurons to the lateral line ganglia that innervate the neuromasts and in the absence of neural crest these ganglia, as well as the lateral line afferent nerves, are disrupted. Finally, we establish that as ontogeny proceeds, the most anterior supraorbital neuromasts come to lie within neural crest-derived frontal and nasal bones in the developing cranium. These are the same anterior supraorbital neuromasts that are absent or mislocated in specimens lacking neural crest cells. Together, our results establish that cranial neural crest and cranial placode derivatives function in concert over the course of ontogeny to build the complex cranial lateral line system.

Pattern formation in the developing hindbrain and cranio-facial region has been studied in a range of vertebrate organisms. The developing hindbrain is transiently segmented into units termed rhombomeres which correspond with domains of gene expression, lineage restriction and neuronal organization and serve to coordinate the migration of cranial neural crest into the adjacent branchial arches. In this paper I review the cellular and molecular events underlying both hindbrain segmentation and the acquisition of segmental identity, consolidating recent results from different model systems. Data suggesting that the vertebrate Hox genes play an important role in specifying positional value to the rhombomeres and cranial neural crest are also examined. I compare expression patterns of the Hox genes between species and consider the mechanisms involved in controlling their appropriate spatial regulation. In addition I describe a recently characterized zebrafish hindbrain segmentation mutant, valentino; morphological, cellular and gene expression data for this mutant are helping to further our understanding of hindbrain patterning.