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    About

Development (Springer)

The Company of Biologists Ltd.

1987-

ISSN: 0950-1991 (1477-9129)
Developmental Biology - Developmental Biology - Molecular Biology
APC costs unknown

Recent articles

1 show abstract
2019-04-01T00:59:40-07:00
Nick Hopwood


Scientific disciplines embody commitments to particular questions and approaches, scopes and audiences; they exclude as well as include. Developmental biology is no exception, and it is useful to reflect on what it has kept in and left out since the field was founded after World War II. To that end, this article sketches a history of how developmental biology has been different from the comparative, human and even experimental embryologies that preceded it, as well as the embryology that was institutionalized in reproductive biology and medicine around the same time. Early developmental biology largely excluded evolution and the environment, but promised to embrace the entire living world and the whole life course. Developmental biologists have been overcoming those exclusions for some years, but might do more to deliver on the promises while cultivating closer relations, not least, to reproductive studies.
2 show abstract
2019-04-04T06:17:20-07:00
Zachary L. Sebo and Matthew S. Rodeheffer


Adipose tissue is composed of anatomically distinct depots that mediate several important aspects of energy homeostasis. The past two decades have witnessed increased research effort to elucidate the ontogenetic basis of adipose form and function. In this Review, we discuss advances in our understanding of adipose tissue development with particular emphasis on the embryonic patterning of depot-specific adipocyte lineages and adipocyte differentiation in vivo. Micro-environmental cues and other factors that influence cell identity and cell behavior at various junctures in the adipocyte lineage hierarchy are also considered.
3 show abstract
2019-04-04T06:17:20-07:00
Tomke Stürner, Anastasia Tatarnikova, Jan Mueller, Barbara Schaffran, Hermann Cuntz, Yun Zhang, Maria Nemethova, Sven Bogdan, Vic Small, and Gaia Tavosanis


The formation of neuronal dendrite branches is fundamental for the wiring and function of the nervous system. Indeed, dendrite branching enhances the coverage of the neuron's receptive field and modulates the initial processing of incoming stimuli. Complex dendrite patterns are achieved in vivo through a dynamic process of de novo branch formation, branch extension and retraction. The first step towards branch formation is the generation of a dynamic filopodium-like branchlet. The mechanisms underlying the initiation of dendrite branchlets are therefore crucial to the shaping of dendrites. Through in vivo time-lapse imaging of the subcellular localization of actin during the process of branching of Drosophila larva sensory neurons, combined with genetic analysis and electron tomography, we have identified the Actin-related protein (Arp) 2/3 complex as the major actin nucleator involved in the initiation of dendrite branchlet formation, under the control of the activator WAVE and of the small GTPase Rac1. Transient recruitment of an Arp2/3 component marks the site of branchlet initiation in vivo. These data position the activation of Arp2/3 as an early hub for the initiation of branchlet formation.
4 show abstract
2019-04-02T08:00:12-07:00
Mitsutomo Abe, Shingo Kosaka, Mio Shibuta, Kenji Nagata, Tomohiro Uemura, Akihiko Nakano, and Hidetaka Kaya


FLOWERING LOCUS T (FT) is an essential component of florigen in Arabidopsis thaliana. Transcription of FT is induced in leaves, and the resulting FT protein is transported to the shoot apex, in which it initiates floral development. Previous analyses suggest that, together with the b-ZIP transcription factor FD, FT regulates the transcription of downstream targets such as APETALA1 (AP1) in floral anlagen. However, conclusive in vivo evidence that FT is transported to the shoot apex to form an FT–FD complex is lacking. Here, using an innovative in vivo imaging technique, we show that the FT–FD complex and AP1 colocalise in floral anlagen. In addition, the FT–FD complex disappears soon after the floral transition owing to a reduction in FD transcripts in the shoot apex. We further show that misinduction of FD activity after the transition leads to defective reproductive development. Taken together, our results indicate that the FT–FD complex functions as a transient stimulus and imply that a regulatory mechanism exists during the floral transition that reduces FT–FD complex levels via modulation of FD expression.
5 show abstract
2019-04-04T06:17:20-07:00
Ashley A. DeAguero, Lizzet Castillo, Sandy T. Oas, Kaveh Kiani, Anton L. Bryantsev, and Richard M. Cripps


Serum response factor (SRF) has an established role in controlling actin homeostasis in mammalian cells, yet its role in non-vertebrate muscle development has remained enigmatic. Here, we demonstrate that the single Drosophila SRF ortholog, termed Blistered (Bs), is expressed in all adult muscles, but Bs is required for muscle organization only in the adult indirect flight muscles. Bs is a direct activator of the flight muscle actin gene Act88F, via a conserved promoter-proximal binding site. However, Bs only activates Act88F expression in the context of the flight muscle regulatory program provided by the Pbx and Meis orthologs Extradenticle and Homothorax, and appears to function in a similar manner to mammalian SRF in muscle maturation. These studies place Bs in a regulatory framework where it functions to sustain the flight muscle phenotype in Drosophila. Our studies uncover an evolutionarily ancient role for SRF in regulating muscle actin expression, and provide a model for how SRF might function to sustain muscle fate downstream of pioneer factors.
6 show abstract
2019-04-04T06:17:20-07:00
Rohan J. Khadilkar and Guy Tanentzapf


Hematopoiesis requires coordinated cell signals to control the proliferation and differentiation of progenitor cells. In Drosophila, blood progenitors, called prohemocytes, which are located in a hematopoietic organ called the lymph gland, are regulated by the Salvador-Warts-Hippo pathway. In epithelial cells, the Hippo pathway integrates diverse biological inputs, such as cell polarity and cell-cell contacts, but Drosophila blood cells lack the conspicuous polarity of epithelial cells. Here, we show that the septate-junction components Cora and NrxIV promote Hippo signaling in the lymph gland. Depletion of septate-junction components in hemocytes produces similar phenotypes to those observed in Hippo pathway mutants, including increased differentiation of immune cells. Our analysis places septate-junction components as upstream regulators of the Hippo pathway where they recruit Merlin to the membrane. Finally, we show that interactions of septate-junction components with the Hippo pathway are a key functional component of the cellular immune response following infection.
7 show abstract
2019-04-04T06:17:20-07:00
Kazuko Hanyu-Nakamura, Kazuki Matsuda, Stephen M. Cohen, and Akira Nakamura


Specification of germ cells is pivotal to ensure continuation of animal species. In many animal embryos, germ cell specification depends on maternally supplied determinants in the germ plasm. Drosophila polar granule component (pgc) mRNA is a component of the germ plasm. pgc encodes a small protein that is transiently expressed in newly formed pole cells, the germline progenitors, where it globally represses mRNA transcription. pgc is also required for pole cell survival, but the mechanism linking transcriptional repression to pole cell survival remains elusive. We report that pole cells lacking pgc show premature loss of germ plasm mRNAs, including the germ cell survival factor nanos, and undergo apoptosis. We found that pgc–
pole cells misexpress multiple miRNA genes. Reduction of miRNA pathway activity in pgc–
embryos partially suppressed germ plasm mRNA degradation and pole cell death, suggesting that Pgc represses zygotic miRNA transcription in pole cells to protect germ plasm mRNAs. Interestingly, germ plasm mRNAs are protected from miRNA-mediated degradation in vertebrates, albeit by a different mechanism. Thus, independently evolved mechanisms are used to silence miRNAs during germ cell specification.
8 show abstract
2019-04-01T00:59:40-07:00
Tanya E. Foley, Bradley Hess, Joanne G. A. Savory, Randy Ringuette, and David Lohnes


Murine cardiac and hematopoietic progenitors are derived from Mesp1+
mesoderm. Cdx function impacts both yolk sac hematopoiesis and cardiogenesis in zebrafish, suggesting that Cdx family members regulate early mesoderm cell fate decisions. We found that Cdx2 occupies a number of transcription factor loci during embryogenesis, including key regulators of both cardiac and blood development, and that Cdx function is required for normal expression of the cardiogenic transcription factors Nkx2-5 and Tbx5. Furthermore, Cdx and Brg1, an ATPase subunit of the SWI/SNF chromatin remodeling complex, co-occupy a number of loci, suggesting that Cdx family members regulate target gene expression through alterations in chromatin architecture. Consistent with this, we demonstrate loss of Brg1 occupancy and altered chromatin structure at several cardiogenic genes in Cdx-null mutants. Finally, we provide evidence for an onset of Cdx2 expression at E6.5 coinciding with egression of cardiac progenitors from the primitive streak. Together, these findings suggest that Cdx functions in multi-potential mesoderm to direct early cell fate decisions through transcriptional regulation of several novel target genes, and provide further insight into a potential epigenetic mechanism by which Cdx influences target gene expression.
9 show abstract
2019-04-11T02:28:22-07:00
Estefania Sanchez-Vasquez, Marianne E. Bronner, and Pablo H. Strobl-Mazzulla


miR-203 is a tumor-suppressor microRNA with known functions in cancer metastasis. Here, we explore its normal developmental role in the context of neural crest development. During the epithelial-to-mesenchymal transition of neural crest cells to emigrate from the neural tube, miR-203 displays a reciprocal expression pattern with key regulators of neural crest delamination, Phf12 and Snail2, and interacts with their 3'UTRs. We show that ectopic maintenance of miR-203 inhibits neural crest migration in chick, whereas its functional inhibition using a ‘sponge’ vector or morpholinos promotes premature neural crest delamination. Bisulfite sequencing further shows that epigenetic repression of miR-203 is mediated by the de novo DNA methyltransferase DNMT3B, the recruitment of which to regulatory regions on the miR-203 locus is directed by SNAIL2 in a negative-feedback loop. These findings reveal an important role for miR-203 in an epigenetic-microRNA regulatory network that influences the timing of neural crest delamination.
10 show abstract
2019-04-05T02:15:52-07:00
Austin Q. Seroka and Chris Q. Doe


The generation of neuronal diversity is essential for circuit formation and behavior. Morphological differences in sequentially born neurons could be due to intrinsic molecular identity specified by temporal transcription factors (henceforth called intrinsic temporal identity) or due to changing extrinsic cues. Here, we have used the Drosophila NB7-1 lineage to address this issue. NB7-1 generates the U1-U5 motor neurons sequentially; each has a distinct intrinsic temporal identity due to inheritance of different temporal transcription factors at its time of birth. We show that the U1-U5 neurons project axons sequentially, followed by sequential dendrite extension. We misexpressed the earliest temporal transcription factor, Hunchback, to create ‘ectopic’ U1 neurons with an early intrinsic temporal identity but later birth-order. These ectopic U1 neurons have axon muscle targeting and dendrite neuropil targeting that are consistent with U1 intrinsic temporal identity, rather than with their time of birth or differentiation. We conclude that intrinsic temporal identity plays a major role in establishing both motor axon muscle targeting and dendritic arbor targeting, which are required for proper motor circuit development.

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Sherpa/Romeo info

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  • Publisher will automatically deposit in PMC for authors funded by RCUK, HHMI, NIH, MRC, Wellcome Trust for release 6 or 12 months after publication
  • Publisher last contacted on 16/11/2015


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APC Discount

For this journal no deals have been made concerning APC discount

More information on Open Access publishing

Impact

Journal Citation Reports (2017)

Impact factor: 5.413
Q1 (Developmental Biology (5/42))

Scopus Journal Metrics (2017)

SJR: 4.698
SNIP: 1.407
Impact (Scopus CiteScore): 0.557
Quartile: Q1
CiteScore percentile: 92%
CiteScore rank: 6 out of 76
Cited by WUR staff: 641 times. (2014-2016)

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