In 2014, the British Society of Developmental Biology (BSDB) has initiated the Gurdon Summer Studentship program with the intention to provide highly motivated students with exceptional qualities and a strong interest in Developmental Biology an opportunity to engage in practical research. Each year, 10 successful applicants spend 8 weeks in the research laboratories of their choices, and the feedback we receive is outstanding. Please, read the student report, kindly sent to us by Isabella Watts(Oxford University) who was hosted in summer 2015 by Tatjana Sauka-Spengler at the Weatherall Institute of Molecular Medicine in Oxford..

A transcriptional analysis of the innate immune response to melanoma: the promise of the zebrafish

This summer I was privileged enough to receive a Gurdon Summer Studentship to work for 8 weeks in the laboratory of Tatjana Sauka-Spengler, at the Weatherall Institute of Molecular medicine. About to go into my third year of studying medicine at Oxford, I have spent the majority of the first two years of my degree learning about the science that underpins medicine. All our lecturers highlight the importance of understanding the scientific evidence that underlies the concepts that we learn. However, no matter how much time you spend trawling through the depths of PubMed to find a new and exciting paper for an essay, it’s not the same as getting hands on experience in a laboratory and learning about different scientific techniques.

My project involved helping my supervisor Amy Kenyon with the final steps of her PhD. Amy had generated a transgenic zebrafish model to study the innate immune response under conditions of inflammation, including tuberculosis and melanoma. This model system harnesses developmental biology and basic science to provide an invaluable tool to better understand the mechanisms of different disease states.

I was mainly focussing on the innate immune response to melanoma, which is an incredibly exciting area of research as macrophages and neutrophils form a major part of the tumour microenvironment. These cells have diverse roles in tumours and can both destroy transformed cells and also contribute to tumour development. However, it has proven difficult to fully examine the interactions of these cells and transformed cells in vivo due to limitations in current model systems. Amy developed a unique model system, pioneered in vivo by the Sauka-Spengler laboratory, which allows isolation of specific cell types and cellular compartments directly from the organism, via a genetically encoded, tissue-specific biotin tagging system.

The system involves fish that ubiquitously express the nuclear envelope-associated protein Rangap fused to an Avi-tag (Avi-Rangap). These have then been crossed with a separate transgenic line where E.coli biotin ligase (BirA) is selectively expressed under control of the mpeg or mpo promoter which are specifically active in macrophages or neutrophils, respectively. Therefore, in the macrophages or neutrophils, biotin is covalently added to the Avi-tag Rangap protein, resulting in the ‘biotinylation’ and tagging of the nuclei of these cells, which can then be isolated using highly stringent streptavidin-biotin affinity purification protocol.

To generate an inducible melanoma model, another binary system of transgenic fish has been used. In the driver line, the bacterial LexPR repressor is fused to a truncated form of the human progesterone receptor, all under the control of a melanocyte specific promoter. The effector line harbours the Lex Operon, controlling the expression of a Ras-oncogene fused to an mCherry fluorescent reporter. When the synthetic steroid mifepristone is added to the water of embryos carrying both alleles, it binds to the LexPR transactivator which, in turn, binds to the Lex Operon region and drives expression of Ras-oncogene specifically in melanocytes, resulting in their transformation and proliferation.

From the very first day of my project I learned a huge amount, and the learning curve was definitely vertical at times! I was incredibly lucky to be working on a very broad topic which meant that I was able to try my hand at a huge number of different techniques.

Some of the earliest work I did involved confirmation of the different model lines I was using. In my first experiment, I wanted to check whether the melanoma model we were using effectively mimicked the cancer over-proliferation phenotype. In the zebrafish embryo melanocytes are usually post-mitotic at 60 hours post fertilisation, thus I wanted to confirm that induction of our cancer system resulted in continued cell proliferation past this point. We injected EdU, a thymidine analogue incorporated into the DNA of dividing cells, into the pericardium of day 4 embryos, in order to label proliferating cells. Upon imaging we saw that, in fish where the LexPR system was activated, there was continued proliferation of melanocytes whilst in control fish there was no overlap between the melanocytes and the stain that labelled the dividing cells.

In the next step of my project I made use of the transparency of the early zebrafish embryo to image the live interaction between the neutrophils, macrophages and transformed melanocytes (Fig. 2). The final step of my project was a transcriptional analysis of the interactions between the innate immune cells and tumour cells. Collecting day 5 embryos where we had induced the oncogenic transformation in melanocytes, we selectively isolated the nuclei of macrophages and neutrophils from the fish using the streptavidin-biotin affinity purification previously mentioned. Whilst incredibly rewarding, this did involve spending entire days in the cold room, and I got a lot of strange looks as I carried 3 jumpers into work in the blazing sun and even drank hot chocolate in the institute’s cafeteria on the hottest day of the year! After isolating the RNA from the nuclei and making cDNA libraries, the data was sent off for sequencing and we were able to see which genes were up- and down-regulated in these cells in response to the cancer.

Looking back at my time in the lab I can’t quite believe how much I have learned! I have had an amazing time and every week has been packed with new things. I loved getting to learn more about the processes involved in laboratory science and I have been convinced that in the future I want to combine both clinical work and research. This has been a very valuable experience and I would really encourage other university students to apply for a Gurdon Summer Studentship. I also want to say a huge thank you to everyone in my lab, especially Tatjana and Amy for making my summer so interesting!

Isabella Watts

(5 votes)

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The Department of Neural Development and Physiology at Institute of Cell Physiology at the National University of Mexico (www.ifc.unam.mx), is seeking for outstanding candidates to apply for a tenure track position equivalent to Assistant Professor. Application deadline: February 29^th , 2016

Candidates must fulfill the following requirements:

• Ph.D. degree.
• Three years (minimum) of postdoctoral experience.
• Excellent academic and publication records (at least 8-10 publications in prestigious journals), showing a record of scientific contributions in areas related to neural development and physiology.
• The proposal should include multidisciplinary experimental approaches and the use of cutting edge techniques.
• To be under 37 years old for men and 39 years old for women at the time of the official incorporation date.
• It is desirable that the candidates are eligible or awardees of grants to establish their own independent laboratory.

Duties:

• To lead a research group with an innovative and independent project.
• To be eager to integrate into a multidisciplinary team and collaborate.
• To obtain external financial support for his/her research.
• To train young researchers at bachelor and graduate levels.
• To communicate his/her discoveries to the society.
• To support the development of the institution.

The Institute will provide:

• Laboratory space
• Access to institutional equipment and service units.
• Salary (depending on applicant qualifications).

Submit your application before February 29^th, 2016 to secdir@ifc.unam.mx and addressed to Dr. Marcia Hiriart Urdanivia Director of the Institute of Cell Physiology, including:

• Cover letter describing research experience and interests, a list of all publications highlighting the most relevant ones with a brief explanation of their importance and PDF of all publications.
• Curriculum vitae
• Three letters of reference or contacts of professionals providing reference letters.
• Research plan (no more than 10 pages)

A copy of the full application should be submitted to seacad@ifc.unam.mx

Selection: a Selection Committee will evaluate Applicants. On April 1st, 2016, selected candidates will be asked to give a seminar at the Institute and will be interviewed by faculty members, any time between April 15^th and May 20^th, 2016.

Selection announcement: not later than June 14^th, 2016.

Position available to start: Between August 16^th and September 16^th, 2016.

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Our group has an opening for a postdoctoral fellow to work on NIH-funded projects involving FGF signaling in cochlear development, with a focus on auditory supporting and sensory cell differentiation in the mouse model. Candidates should have >2 years of graduate or postdoctoral research experience in inner ear development, including anatomic, molecular and functional analyses, with strong publications (can be pending) in these areas. Individuals with expertise in confocal microscopy of other developing and mature sensory systems with an interest in studying the ear are also encouraged to apply. Experience with mouse genetics is not absolutely required, but is a big plus. The stipend will follow NIH guidelines. Benefits include health and dental insurance. The successful candidate will be mentored through the process of applying within two years of the initial appointment for individual support (for stipend and/or newly developed project) as appropriate. Presentation and networking opportunities include a weekly Human Genetics Research-in-Progress series and a monthly meeting of the Inner Ear Research Group. There will also be an opportunity to attend at least one appropriate scientific conference per year.

If interested, please contact suzi.mansour@genetics.utah.edu and provide a very brief (<1 page) current research description, a Biosketch, and the names and contact information of two individuals (current PI and one other), who can be contacted to comment on your suitability for this position. The position can start as early as Jan. 4, 2016, but other start dates are negotiable.

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In 2014, the British Society of Developmental Biology (BSDB) has initiated the Gurdon Summer Studentship program with the intention to provide highly motivated students with exceptional qualities and a strong interest in Developmental Biology an opportunity to engage in practical research. Each year, 10 successful applicants spend 8 weeks in the research laboratories of their choices, and the feedback we receive is outstanding.

Please, read the student report which was kindly sent to us by Aran Shaunak. Arun studies at Cambridge University and was hosted in summer 2015 by Jose Silva at the Cambridge Stem Cell Institute. During his project, entitled “The molecular mechanisms of Oct4”, Arun aimed to create new cell lines for the study of Oct4 and optimise a protocol for P-STAT3 western blots to test its functional involvement. Arun’s report does not focus on the actual project but rather presents an entertaining opinion piece about the emotional roller coaster of his project, which provides good insights into the realities of laboratory life.

What every potential academic needs to learn about science

(6 votes)

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Disease Models & Mechanisms invites you to submit original research for consideration for an upcoming Special Collection named Spotlight on Rat: Translational Impact scheduled for publication in autumn 2016. This ongoing collection* will focus on translational advances made using Rat as a model organism, including insights into disease mechanisms and therapeutic targets, new resources and technologies, and drug discovery and development.

The issue will be guest edited by Tim Aitman (University of Edinburgh, UK)

We invite you to showcase your breakthrough Rat research in this Special Collection. Submissions should describe original research in the form of a Research or Resource article. Please read the author guidelines for information on preparing a manuscript for DMM, and submit your manuscript via our online submission system. Please highlight that your submission is to be considered for the Special Collection in your cover letter. For rapid feedback on the suitability of a paper for inclusion in the Special Collection, please send us a presubmission enquiry. The Collection will also contain invited Review articles covering topics of broad interest to the Rat community and interviews with leading scientists in the field. The launch issue of the Special Collection will be widely marketed and will be distributed at relevant conferences worldwide, providing prominent exposure for your work.

Submission deadline: 1st March 2016

Key benefits of publishing in DMM include:

• High visibility and impact (2014 Impact Factor 5)
• Open Access (CC-BY licence) and PMC deposition
• Rapid peer review and publication
• Indexed in Medline, ISI and Scopus
• Not-for-profit publisher

*Please note that not all papers accepted for publication after peer review will be included in the launch issue for the Special Collection; some will be published in later issues and added to the compiled online Special Collection. Contact us for further details.

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In 2014, the British Society of Developmental Biology (BSDB) has initiated the Gurdon Summer Studentship program with the intention to provide highly motivated students with exceptional qualities and a strong interest in Developmental Biology an opportunity to engage in practical research. Each year, 10 successful applicants spend 8 weeks in the research laboratories of their choices, and the feedback we receive is outstanding. Please, read the student report, kindly sent to us by Anna Klucnika who studies at Cambridge University and was hosted in summer 2015 by Aziz Aboobaker in Oxford.

Immortal worms

The Gurdon Summer Studentship has allowed me to undertake a fascinating summer project in the laboratory of Aziz Aboobaker in Oxford, working with the planarian Schmidtea mediterranea, an exciting model for stem cells, ageing and cancer¹. These flatworms have the capacity to regenerate completely from the smallest fragment from almost any body part, owing to the widespread abundance of neoblasts in their mesenchyme. Neoblasts, or at least a subset, have been demonstrated to be pluripotent by single cell injection into lethally irradiated worms resulting in complete rescue².

Since vertebrates do not have adult stem cells that are pluripotent, planarians provide a unique opportunity to study the mechanisms of stem cell maintenance, induction of differentiation, whole body regeneration, as well cancer related stem cell behaviour.

An interesting feature of neoblasts is the presence of chromatoid bodies, which strikingly resemble germ granules found in germ cells across metazoa. These are electron dense structures made up of RNPs involved in posttranslational gene regulation in the germline. Chromatoid bodies and germ granules contain many homologous proteins, which suggests a conserved germline multipotency program³. Except for Nanos, neoblasts express most germ line specific genes, such as homologues to Bruli, Piwi, and Tudor, and RNAi depletion of these proteins blocks regeneration and indicates involvement in neoblast maintenance and differentiation⁴.

Does Tudor reign over pluripotency?

The focus of my project was on the Tudor homologue in S.mediterranea, Smedtud-1. RNAi in a related species, S. polychroa, results in neoblast depletion, indicating a role in long-term neoblast maintenance⁵. From studies in other organisms we know that the Tudor domains of Tudor bind symmetrically dimethylated arginines of Piwi proteins and glycolytic enzymes in the germ granules^6,7. These studies and knockdowns indicate that Tudor is involved in piRNA synthesis required for gametogenesis and stem cell maintenance. The role that Tudor may have as a pluripotency factor made me keen to investigate this mysterious protein.

What makes the picture even more interesting is that RNP granules are also found in planarian neurons and Smedtud-1 is expressed in the CNS as well as in germ cells and neoblasts^8,9. However it is not known in which specific neurons Tudor is expressed or when Tudor expression is switched on and/or off.

Elucidating the Tudor lineage

I wanted to find out what is the pattern of Tudor expression in stem cell progeny as they differentiate into neurons. To do this I carried out fluorescence in situ hybridization (FISH) for several markers (tudor, coe, th, tph, ChAT¹⁰) to visualize their expression on top of an immunostain for Tudor protein.

Coe is a marker for neural progenitors and neurons and so I synthesised antisense probes to detect coe to see whether Tudor is co-expressed continuously throughout the neuronal lineage or not.

To establish where in the CNS Tudor is expressed, various markers for specific neuronal subtypes were used- th for dopaminergic, tph for serotonergic and ChAT for cholinergic neurons. Anish, a DPhil student, was thus able to help me show that Tudor protein is not expressed, for example, in dopaminergic neurons but in proximal neurons.

To find out whether the expression pattern of the transcript matches that of Tudor protein. I used the genome data available to clone Smedtud-1 to synthesise antisense probes that I used for FISH jointly with immunostaining for the protein using the Tudor antibody.

Although I wasn’t able to collect all of my data in the short time that I was in the lab, I’ve achieved so much. I’ve learnt how to cut worms, microinject, clone genes, synthesise probes and carry out immuno and in situ protocols. I’ve learnt to always ask when in doubt. I’ve learnt to be scrupulous. I’ve learnt that it can be very frustrating when experiments don’t work out as planned and when time runs out. But those little setbacks showed me just how determined I am to do science.

The Aboobaker lab was extremely welcoming and supportive. Thank you to Aziz, Natasha, Dani, Nobu, Prasad, Anish, Sounak, Yuli, Sam, Damian, Alvina, Holly, Ben and Alex.

(7 votes)

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Our jobs page was very busy this month! Check out the 13 new positions available. Elsewhere on the Node:

Research:

– Mike Levin explains how his group used artificial intelligence to produce a model that explains the all-or-none phenotypes seen in depolarised Xenopus tadpoles.

– How do you express two genes stably and bicistronically through electroporation in chick? Joana Lima posted about her recent paper in BMC Developmental Biology.

– Julia posted a new stem cell image, and told us a bit about pancreas development!

Discussion:

– The New Year is coming! What is your wish list for your research in the year 2016? Tell us in the latest question of the month!

– Why was Micrographia such an important book? Cat Vicente posted about why scientists should know about Robert Hooke’s work.

Also on the Node:

– Marcela told us about the time she spent in Jeremy Brocke’s lab in UCL and her visit to the lab of Aziz Aboobaker at the University of Oxford, sponsored by a Development Travelling Fellowship.

– An interview with José Silva featured in the Node this month!

– A new Mole cartoon, about grant writing (and proposing to Fundamentally Change the World As We Know It). And two more Sticky Wicket posts on bad and not-so-bad ideas.

– Check out the SDB’s new small grants program!

– And Oliver Davis wrote about his time at Jean-Paul Vincent’s lab sponsored by a BSDB Gurdon Studentship!

Happy reading!

(1 votes)

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Here are the highlights from the current issue of Development:

Human embryos: a mixed bag

Human embryonic stem cells (hESCs) are conventionally derived from embryos that are at the blastocyst stage of development. Now, to gain insight into lineage allocation in early human development, Susan Fisher and colleagues report the derivation of various hESC lines using single blastomeres from 8- and 12-cell human embryos (p. 4010). The characterisation of these lines reveals that, at the transcriptome level, they differ from blastocyst-derived lines. Notably, blastomere-derived hESCs are enriched for genes expressed by trophoblasts and the ectoplacental cone. The researchers further show that blastomere-derived lines are hypomethylated in genomic regions that control trophoblast differentiation and early developmental processes, indicative of trophoblast competence. Variations in gene expression profiles are also observed among the various blastomere-derived lines (all of which are derived from embryos from a single couple), highlighting the existence of blastomere heterogeneity. In line with this, the authors show that levels of EOMES, T, GDF15 and active b-catenin differ among the blastomeres of 8- to 10-cell human embryos. Finally, the researchers report the derivation of the first human trophoblast stem cell line, which could be used in the future to model placental development and disorders.

Cilia: at the heart of chamber maturation

Increasing evidence suggests that blood flow and biomechanical forces generated by the developing heart feedback to regulate cardiac chamber formation and maturation. How such forces are sensed and translated, however, remains unclear. Here, Jiandong Liu and co-workers show that, in zebrafish, cardiac contraction activates Notch signalling in the endocardium to control chamber maturation (p.4080). By analysing embryos deficient for troponin T type 2a (tnnt2a), which encodes an essential component of the cardiac contraction apparatus, the researchers first show that cardiac contraction is required for the formation of cardiac trabeculae – the luminal protrusions that are indicative of cardiac chamber maturation. They further show that cardiac contraction controls Notch signalling in the endocardium; notch1b expression is reduced in tnnt2a^–/– embryos. Notch activation, they report, induces the expression of ephrin b2a and neuregulin 1 to promote trabeculation. Finally, the authors demonstrate that shear stress controls notch1b expression in a primary cilia-dependent manner, suggesting that primary cilia in this context are responsible for detecting fluid flow. In summary, these findings highlight a molecular mechanism that links flow sensing to the transcriptional changes that regulate cardiac development.

Vascular development in full flow

Vascular development and angiogenesis are known to be regulated by various signals, but the roles played by blood flow and biomechanical signals are unclear. This is mostly because the ability to image and measure changes in blood flow has been limited. Now, Elizabeth Jones and colleagues develop a method to simultaneously image blood flow dynamics and vascular remodelling (p. 4158), and use this technique to show that flow dynamics control sprout location and elongation in quail embryos (p.4151). Their imaging approach uses micro-particle image velocimetry: embryos are injected with a fluorescent dye that labels endothelial cells and with fluorescent microspheres that act as tracers of fluid motion. Subsequent imaging via a high-speed camera allows changes in blood flow dynamics and vessel geometry to be quantified. Using this method, the researchers demonstrate that sprout location can be predicted based on flow dynamics; sprouts form from vessels that are at a lower pressure towards vessels at a higher pressure and localise to points where shear stress, a force created by flow, is at a minimum. In addition, the rate of sprout elongation is proportional to the pressure difference between the two vessels. These studies provide insights into the hemodynamic forces at play during vascular development and open the door to further studies of the biomechanical control of vascular remodelling.

Con-Nek-ting cilia biogenesis and resorption

The left-right organiser (LRO) is a transient ciliated structure that plays a key role in establishing left-right (LR) asymmetry in the vertebrate embryo. However, the mechanisms that control the formation and resorption of cilia on this structure are unclear. In this issue (p. 4068), Martina Brueckner and colleagues reveal that Nek2 regulates cilia biogenesis and resorption at the Xenopus LRO. They show that both the knockdown and the overexpression of nek2, which encodes a NIMA-like kinase, result in reduced cilia numbers and motility at the LRO and hence abnormal LR development. Nek2 is known to play a role in centriole separation and, in line with this, the authors reveal that the knockdown of nek2results in centriole defects in the LRO. They further show that Nek2 acts upstream of the tubulin deacetylase Hdac6, and that it interacts with the nucleoporin Nup98, to control cilia resorption. Together, these findings demonstrate that Nek2 is involved in multiple stages of the cilia life cycle. Given that NEK2 has previously been implicated in abnormal laterality in humans, these findings also provide further evidence that links Nek family kinases to human ciliopathies.

An appendage to Hox gene function

Hox genes are best known for their role in axial patterning during embryogenesis, but they have also been implicated in the development and patterning of cutaneous accessory organs, such as hair follicles and mammary glands. How do they function in this context? Here, by showing that Hoxc8 can initiate an ectopic mammary gland programme in mice, Lara Carroll and Mario Capecchi propose that Hox genes regulate the distribution of cutaneous appendages (p. 4056). They first show that Hoxc8 is transiently expressed in the early surface ectoderm prior to mammary line formation. The researchers then show that the conditional overexpression of Hoxc8 – to express it in regions where it is not normally expressed – results in the formation of ectopic mammary placodes. These ectopic rudiments express known mammary placode markers, such as Tbx3 and Wnt10b. The authors further report that the ablation of ectodermal Tbx3 prevents the formation of both normal and ectopic mammary rudiments, suggesting that Tbx3 is directly regulated by Hoxc8 during mammary development. Together, these and other findings highlight a role for Hoxc8 in the initial stages of mammary development and suggest that Hoxc8 and other Hox genes play roles during the regional specification of cutaneous appendages.

PLUS…

How to make an oligodendrocyte

The loss of oligodendrocytes – the cells that produce the myelin sheath of axons – can result in a broad array of diseases including cerebral palsy and multiple sclerosis. Accordingly, replacing lost oligodendrocytes holds great promise as a therapeutic strategy. Here, Goldman and Kuypers describe the molecular events regulating oligodendrocyte development in vivo and discuss how our understanding of this process has led to the establishment of methods for producing oligodendrocytes in vitro. See the Primer on p. 3983

*Also see the other articles in the “How to make…” series here

Morphogen rules: design principles of gradient-mediated embryo patterning

The Drosophila blastoderm and the vertebrate neural tube are archetypal examples of morphogen-patterned tissues that create precise spatial patterns of different cell types. Here, James Briscoe and Stephen Small compare these systems in the context of gene regulatory networks and dynamical systems theory. This comparison reveals several shared features that suggest that a set of common design principles underpins the patterning of both tissues. See the Review on p. 3996

(No Ratings Yet)

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It’s getting to that time of year when we think about the year to come and the things we hope it will bring: love, health, money… and maybe a little bit of help with our research.

There are many things that could make the year 2016 better for a developmental scientist: new equipment, better protocols, an easier way to maintain a model organism, or quite simply some more time to do experiments! So, in the spirit of the festive season, this month we are asking:

What is your research wish list for the New Year?

Share your thoughts by leaving a comment below! You can comment anonymously if you prefer. We are also collating answers on social media via this Storify. And if you have any ideas for future questions please drop us an email!

(2 votes)

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Here is some developmental biology related content from other journals published by The Company of Biologists.

Genome-wide lacZ profiling in the mouse

Tuck, Estebel and colleagues have produced an open access adult mouse expression resource with the expression profile of 424 assessed in up to 47 different organs, tissues and substructures using a lacZ reporter gene. Read the paper here [OPEN ACCESS].

A method for labelling leukocytes infiltrating the mouse retina

Sim and colleagues describe a method to image myeloid cells infiltrating the mouse retina in vivo using a depot injection of indocyanine green dye (ICG). Read the paper here [OPEN ACCESS].

Urine-derived stem cells predict patient response to cholesterol-lowering drug

Si-Tayeb, Idriss and colleagues have shown that cells derived from patient urine samples can be reprogrammed to generate patient-specific models of hypercholesterolemia, providing a tool to predict patient response to cholesterol-lowering drugs. Read the paper here [OPEN ACCESS], and read the press release here.

Mass and drought resistance linked in seedlings

Seedlings of large-seeded plants are considered to withstand abiotic stress more efficiently. Meng and colleagues show that the integration of drought stress response into the regulation of mass is mediated by the transcription factor ARF2. Read the paper here.

New role for eIF6 in myofibroblast differentiation

Myofibroblast differentiation is regulated by TGF-β1. In this paper, Yang and colleagues show that eukaryotic initiation factor 6 can modulate myofibroblast differentiation by altering the occupancy of the TGF-β1 promoter by H2A.Z and Sp1, affecting TGF-β1 transcription. Read the paper here.

High-salt exposure increases cardiovascular defects in early chick embryos

In chick, embryonic mortality at early stages is usually due to vascular malformations. Wang and colleagues show that high-salt exposure results in angiogenesis and heart defects, possibly due to excess generation of reactive oxygen species (ROS). Read the paper here.

The effects of rearing amphibious fish out of water

Wells, Turko and Wright rear an amphibious fish in and out of water, and find that embryos reared in aqueous environments consume more energy than their faster developing terrestrial counterparts. Read the paper here.

Hatching success does not decrease with higher nest temperatures in flatback turtles

Elevated nest temperatures caused by climate change could harm the viability of ectotherm eggs. Howard and colleagues show that high nest temperatures do not decrease hatching success in flatback turtles, and observe a high pivotal sex-determining temperature in these turtles. Read the paper here.

(1 votes)

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