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Register for On Demand Access to @keystoneSymposia.bsky.social #SystemsImmunology to #Immunoengineering to explore emerging research #KSSysImmune26

Visit hubs.la/Q03VtR690 and click on Pricing & Registration

10 hours ago 0 0 0 0
Microscopy images showing glomerular microthrombi in the kidney cortex of mice treated with medium‑chain or long‑chain polyphosphates (P100 or P700), alone or combined with LPS. (A) Masson’s trichrome staining highlights red fibrin deposits and blue collagen deposits within glomerular capillary loops, most prominent in P700 and LPS+P700 groups. (B) Immunofluorescence images show red CD61‑positive platelets accumulating in glomeruli and arterioles, with green LTL marking proximal tubule brush borders and blue Hoechst staining nuclei. Insets display individual and merged channels. (C) High‑magnification immunofluorescence shows red von Willebrand factor–positive deposits in glomerular capillary loops of P700 and LPS+P700 mice, with green nephrin showing a granular podocyte pattern and blue Hoechst‑stained nuclei.

Microscopy images showing glomerular microthrombi in the kidney cortex of mice treated with medium‑chain or long‑chain polyphosphates (P100 or P700), alone or combined with LPS. (A) Masson’s trichrome staining highlights red fibrin deposits and blue collagen deposits within glomerular capillary loops, most prominent in P700 and LPS+P700 groups. (B) Immunofluorescence images show red CD61‑positive platelets accumulating in glomeruli and arterioles, with green LTL marking proximal tubule brush borders and blue Hoechst staining nuclei. Insets display individual and merged channels. (C) High‑magnification immunofluorescence shows red von Willebrand factor–positive deposits in glomerular capillary loops of P700 and LPS+P700 mice, with green nephrin showing a granular podocyte pattern and blue Hoechst‑stained nuclei.

Long-chain #polyphosphates play a procoagulant role in #kidney injury by inducing microthrombi characteristic of thrombotic microangiopathy and augmenting cytokine levels under inflammatory conditions.

A. Pirttiniemi, N. Sandholm, M. Lehto & co
@finndiane.bsky.social
doi.org/10.1242/dmm....

1 day ago 0 0 0 0
Figure illustrating a workflow to measure neuronal activity in C. elegans using GCaMP6m fluorescence and microfluidic immobilization. A: Confocal images of a 4‑day‑old worm expressing pan‑neuronal GCaMP6m, shown at whole‑animal and head‑region magnification. B: Diagram of the PDMS microfluidic device that straightens and traps worms for imaging, with a magnified view of animals inside the channels. C: Overview of the workflow: imaging age‑synchronized animals, quantifying GCaMP6m fluorescence from snapshots, and normalizing values using GCaMP6m protein levels measured by western blot. D: Violin plot showing reduced neuronal GCaMP6m fluorescence in unc‑13 mutants compared with controls. E: Scatter plot showing lower GCaMP6m protein levels in unc‑13 mutants. F: Violin plot of fluorescence normalized to protein levels, again showing reduced neuronal activity in unc‑13 mutants.

Figure illustrating a workflow to measure neuronal activity in C. elegans using GCaMP6m fluorescence and microfluidic immobilization. A: Confocal images of a 4‑day‑old worm expressing pan‑neuronal GCaMP6m, shown at whole‑animal and head‑region magnification. B: Diagram of the PDMS microfluidic device that straightens and traps worms for imaging, with a magnified view of animals inside the channels. C: Overview of the workflow: imaging age‑synchronized animals, quantifying GCaMP6m fluorescence from snapshots, and normalizing values using GCaMP6m protein levels measured by western blot. D: Violin plot showing reduced neuronal GCaMP6m fluorescence in unc‑13 mutants compared with controls. E: Scatter plot showing lower GCaMP6m protein levels in unc‑13 mutants. F: Violin plot of fluorescence normalized to protein levels, again showing reduced neuronal activity in unc‑13 mutants.

Monitoring neuronal activity in #Celegans Alzheimer's model using GCaMP and microfluidic device showed that Aβ and Tau expression reduce neuronal activity and function in young adults, well before amyloid aggregates accumulate.

F. Hirsch, @kirsteinlab.bsky.social & co
Read: doi.org/10.1242/dmm....

4 days ago 1 0 0 0
spotLights Ep 19: preLights in conversation with Kristine Willis
spotLights Ep 19: preLights in conversation with Kristine Willis YouTube video by The Company of Biologists

How do funding decisions shape the direction of biomedical research? Can we spot transformative discoveries years before they are recognised by prizes, policies, or the wider community?

Watch the #spotLights discussion feat. @kawillis.bsky.social & @jontytownson.bsky.social
youtu.be/u-X3dYl7dHQ?...

5 days ago 6 3 0 1
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Check out our interview with the first author, Melody Hancock.

My research uses zebrafish as a model to understand what goes wrong at the molecular level in this [CHARGE] disorder, with the goal of identifying possible new treatment strategies.

Full interview: doi.org/10.1242/dmm....

5 days ago 1 0 0 0
A figure showing transcriptomic and proteomic differences caused by chd7 loss. Panels A and B display principal component analyses: panel A separates RNA samples by genotype and replicate, and panel B shows similar separation for protein samples. Panels C and D show heatmaps: panel C presents clustered log2‑scaled expression of 1,780 differentially expressed genes, and panel D shows clustered expression of 553 differentially expressed proteins. In both heatmaps, heterozygous and homozygous mutants are visually distinct from wild‑type samples.

A figure showing transcriptomic and proteomic differences caused by chd7 loss. Panels A and B display principal component analyses: panel A separates RNA samples by genotype and replicate, and panel B shows similar separation for protein samples. Panels C and D show heatmaps: panel C presents clustered log2‑scaled expression of 1,780 differentially expressed genes, and panel D shows clustered expression of 553 differentially expressed proteins. In both heatmaps, heterozygous and homozygous mutants are visually distinct from wild‑type samples.

Using #zebrafish model of CHARGE, a rare developmental disorder caused by CHD7 mutations, researchers identified dysregulated pathways and candidate genes associated with disease-related phenotypes.

Authors: Melody Hancock, Kurt Marsden & co
@ncstate.bsky.social

Paper: doi.org/10.1242/dmm....

5 days ago 1 0 1 1
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Tanner Robertso, the first author, answered our questions about the research.

'DMM [...] has a great reputation for scientific rigour, and a lot of great zebrafish papers get published here.'

Full interview: doi.org/10.1242/dmm....

6 days ago 0 0 0 0
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Time‑lapse and confocal images of zebrafish larval skin show that xylazine treatment rapidly induces keratinocyte extrusion, tissue‑wide contraction of the post‑anal fin fold, and disruption of basal keratinocyte adhesions. Bright‑field panels highlight increased extrusions and fin‑fold contraction compared with controls, while reporter‑line fluorescence images show keratinocytes leaving the epidermis and selective disorganisation of the basal layer. Quantification plots display increased extrusion events and reduced fin‑fold area after xylazine exposure, with partial rescue by para‑aminoblebbistatin. Additional imaging of F‑actin dynamics reveals loss of intercellular adhesions and eventual de‑adherence of neighbouring basal keratinocytes.

Time‑lapse and confocal images of zebrafish larval skin show that xylazine treatment rapidly induces keratinocyte extrusion, tissue‑wide contraction of the post‑anal fin fold, and disruption of basal keratinocyte adhesions. Bright‑field panels highlight increased extrusions and fin‑fold contraction compared with controls, while reporter‑line fluorescence images show keratinocytes leaving the epidermis and selective disorganisation of the basal layer. Quantification plots display increased extrusion events and reduced fin‑fold area after xylazine exposure, with partial rescue by para‑aminoblebbistatin. Additional imaging of F‑actin dynamics reveals loss of intercellular adhesions and eventual de‑adherence of neighbouring basal keratinocytes.

A #zebrafish model suggests that the veterinary sedative #xylazine disrupts #skin homeostasis through a direct effect on epithelial cells and the kappa‑opioid receptor.

Authors: Tanner Robertson, Anna Huttenlocher & co
@uwmadisonmmi.bsky.social

Full paper: doi.org/10.1242/dmm....

6 days ago 3 1 1 1
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Claudia Müller-Sánchez and María Gertrudis Muñiz-Banciella, the first co-authors, talked to us about their paper.

Its focus on technically solid, broad and useful resources made DMM a natural and ideal home for our study.

Full interview: doi.org/10.1242/dmm....

1 week ago 0 0 0 0
A schematic shows the workflow for isolating and immortalising postnatal RFP‑positive cardiac stromal cells from Wt1GFP/+;Wt1Cre;ROSA26‑tdRFP mice, excluding endothelial (CD31+), hematopoietic (CD45+), and highly GFP‑expressing cells. Adjacent bright‑field images display primary and immortalised RFP‑positive cardiac cells. Additional immunofluorescence panels show strong vimentin expression in immortalised cells and patches of α‑SMA–positive cells visualised with α‑SMA (green) and phalloidin (red).

A schematic shows the workflow for isolating and immortalising postnatal RFP‑positive cardiac stromal cells from Wt1GFP/+;Wt1Cre;ROSA26‑tdRFP mice, excluding endothelial (CD31+), hematopoietic (CD45+), and highly GFP‑expressing cells. Adjacent bright‑field images display primary and immortalised RFP‑positive cardiac cells. Additional immunofluorescence panels show strong vimentin expression in immortalised cells and patches of α‑SMA–positive cells visualised with α‑SMA (green) and phalloidin (red).

A new mouse model enables lineage tracing and visualisation of WT1‑expressing cells, with WT1‑lineage cells marked by RFP and actively WT1‑expressing cells - by GFP.

Authors: Müller-Sánchez, Muñiz-Banciella, Reina, Soriano, Martínez-Estrada
bsky.app/profile/ibub...

Paper: doi.org/10.1242/dmm....

1 week ago 2 0 1 0
How important do you feel discovery research and ‘basic’ science is for understanding disease? Well, I have a little bit of a biased view on the topic, since I'm a basic scientist myself. The lab has made more and more discoveries with very strong therapeutic implications, and often people ask me why we are not pursuing these further ourselves. Part of it is that I think about this very much as an ecosystem. People have different skills – I have colleagues who are very good at the application side of things and I have other colleagues, including people in my lab, who are very good at the basic science. There are a lot of very smart people at every stage in the ecosystem and, sometimes, we have to acknowledge that we can't all be experts in every step. A lot of basic science discoveries will end up having profound implications in the clinic – if you don't have the full imagination about how to get it there, that's okay, because you're still a very important piece of the jigsaw puzzle and other people can help. If the basic science discoveries didn't exist, then it's quite possible that the well would run dry. We cannot simply rely on the idea that the therapies currently in clinical trials are going to be enough because we already know that – for diseases, such as cancer, and with rapidly evolving viruses – there needs to be a constant influx of new ideas to stay ahead of the arms race. I'd also make a plug for the fact that, ultimately, we are all interested in human disease, but disease research in humans is not ethical or possible. This is why creating and studying model organisms in a high-throughput, low-investment context is incredibly important. We cannot just say ‘okay, we're going to stop work on anything that is not related to human research’, because – actually – it's all relevant to humans.

How important do you feel discovery research and ‘basic’ science is for understanding disease? Well, I have a little bit of a biased view on the topic, since I'm a basic scientist myself. The lab has made more and more discoveries with very strong therapeutic implications, and often people ask me why we are not pursuing these further ourselves. Part of it is that I think about this very much as an ecosystem. People have different skills – I have colleagues who are very good at the application side of things and I have other colleagues, including people in my lab, who are very good at the basic science. There are a lot of very smart people at every stage in the ecosystem and, sometimes, we have to acknowledge that we can't all be experts in every step. A lot of basic science discoveries will end up having profound implications in the clinic – if you don't have the full imagination about how to get it there, that's okay, because you're still a very important piece of the jigsaw puzzle and other people can help. If the basic science discoveries didn't exist, then it's quite possible that the well would run dry. We cannot simply rely on the idea that the therapies currently in clinical trials are going to be enough because we already know that – for diseases, such as cancer, and with rapidly evolving viruses – there needs to be a constant influx of new ideas to stay ahead of the arms race. I'd also make a plug for the fact that, ultimately, we are all interested in human disease, but disease research in humans is not ethical or possible. This is why creating and studying model organisms in a high-throughput, low-investment context is incredibly important. We cannot just say ‘okay, we're going to stop work on anything that is not related to human research’, because – actually – it's all relevant to humans.

Do you think basic science is particularly threatened by cuts to funding? Science itself is quite uncertain. We do experiments wondering if they will even work. It's discovery, and you don't know where it's going to lead. It could lead to a billion-dollar company, something like mRNA vaccines or CRISPR-Cas9 gene editing, or it could simply be something that interests you. Sometimes it might appear esoteric from the outside, but there are very smart people dedicated to this work. We shouldn't lose sight of the fact that most of this work is paid for by taxpayers, but funding uncertainty creates a very unstable foundation. If the foundations are weak, people are going to get much more conservative about the science that they're doing and worry that ‘blue-skies research’ is not worth pursuing because it won't get funded. And that would be a mistake because all innovation in science really originates from blue-skies, basic research. The second thing that uncertainty does is send a message to our young trainees – who are our future – that this is not a career option that will provide professional and personal stability. I worry that this kind of uncertainty will mean we lose an entire generation of people, and that would be a loss we might not be able to overcome.

Do you think basic science is particularly threatened by cuts to funding? Science itself is quite uncertain. We do experiments wondering if they will even work. It's discovery, and you don't know where it's going to lead. It could lead to a billion-dollar company, something like mRNA vaccines or CRISPR-Cas9 gene editing, or it could simply be something that interests you. Sometimes it might appear esoteric from the outside, but there are very smart people dedicated to this work. We shouldn't lose sight of the fact that most of this work is paid for by taxpayers, but funding uncertainty creates a very unstable foundation. If the foundations are weak, people are going to get much more conservative about the science that they're doing and worry that ‘blue-skies research’ is not worth pursuing because it won't get funded. And that would be a mistake because all innovation in science really originates from blue-skies, basic research. The second thing that uncertainty does is send a message to our young trainees – who are our future – that this is not a career option that will provide professional and personal stability. I worry that this kind of uncertainty will mean we lose an entire generation of people, and that would be a loss we might not be able to overcome.

I was interviewed by @katiepickup.bsky.social recently for @dmmjournal.bsky.social. This has a little bit of my background, a little bit on science and mentoring, and a little bit (ok, more than a little bit) on funding in science.

Check it out at: journals.biologists.com/dmm/article/...

1 week ago 74 34 2 7
Multi‑panel figure illustrating effects of reducing mutant huntingtin in striatal somatostatin interneurons (SST‑INs). (A) Diagram of AAV9‑SST‑eGFP injection site in the mouse striatum for control, BACHD, and BACHD/SST‑Cre genotypes. (B) Confocal images show SST‑INs expressing eGFP (green) and SST immunolabeling (red), confirming targeted expression; nuclei in blue; 10 µm scale bar. (C) Scatter/violin plot shows higher spontaneous firing rates in BACHD SST‑INs compared with controls, with firing normalized in BACHD/SST‑Cre mice; points indicate mice and lines the median. (D) Example color‑coded traces of spontaneous firing. (E) Cumulative distributions of inter‑event intervals show increased inhibitory synaptic event frequency in BACHD/SST‑Cre SST‑INs. (F) Cumulative distributions of inhibitory postsynaptic current amplitudes show reduced amplitudes in BACHD mice and normalization in BACHD/SST‑Cre mice. (G) Example inhibitory synaptic current traces. (H) Amplitude–frequency histograms

Multi‑panel figure illustrating effects of reducing mutant huntingtin in striatal somatostatin interneurons (SST‑INs). (A) Diagram of AAV9‑SST‑eGFP injection site in the mouse striatum for control, BACHD, and BACHD/SST‑Cre genotypes. (B) Confocal images show SST‑INs expressing eGFP (green) and SST immunolabeling (red), confirming targeted expression; nuclei in blue; 10 µm scale bar. (C) Scatter/violin plot shows higher spontaneous firing rates in BACHD SST‑INs compared with controls, with firing normalized in BACHD/SST‑Cre mice; points indicate mice and lines the median. (D) Example color‑coded traces of spontaneous firing. (E) Cumulative distributions of inter‑event intervals show increased inhibitory synaptic event frequency in BACHD/SST‑Cre SST‑INs. (F) Cumulative distributions of inhibitory postsynaptic current amplitudes show reduced amplitudes in BACHD mice and normalization in BACHD/SST‑Cre mice. (G) Example inhibitory synaptic current traces. (H) Amplitude–frequency histograms

In a new paper, Jahmel Fowler, Michelle Gray & co show that mutant huntingtin expression in somatostatin-expressing interneurons contributes to anxiety-like behavior in male mouse model of #HuntingtonsDisease

doi.org/10.1242/dmm....
#UABMedicine

1 week ago 1 0 0 0
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Metabolic Disorders | Disease Models & Mechanisms | The Company of Biologists Metabolic disorders, such as obesity and type 2 diabetes, have become epidemic in the Western world. Although it is clear that genetics, environmental cues

We are delighted to be media partners with @dmmjournal.bsky.social for our 4th Metabolism in Health & Disease Conference on 10-13 October.

Check out their Metabolic Disorders subject collection:
journals.biologists.com/dmm/collecti...

1 week ago 1 1 0 0
Domain architecture of the heat shock transcription factor (HSF) family of transcription factors. All somatic HSF proteins contain an amino-terminal, winged helix-turn-helix DNA-binding domain (DBD). Downstream of the HSF1, HSF2 and HSF4 DBDs are heptad repeat (HR) regions (HR-A/B) that form the leucine zipper (LZ) domains, with LZ1-3 required for HSF oligomerization. A third HR region (HR-C), which forms LZ4, suppresses HSF activity through intramolecular interactions with LZ1-3 in HSF1 and HSF2. Transcriptional activity for some HSFs requires the activation domain (AD). Sequence similarity was determined using Clustal Omega Multiple Sequence Alignment with protein amino acid sequences obtained from Ensembl. Sequence similarity is scored from 0 to 10, which is indicated by the height and color of the bars under the respective HSF diagrams.

Domain architecture of the heat shock transcription factor (HSF) family of transcription factors. All somatic HSF proteins contain an amino-terminal, winged helix-turn-helix DNA-binding domain (DBD). Downstream of the HSF1, HSF2 and HSF4 DBDs are heptad repeat (HR) regions (HR-A/B) that form the leucine zipper (LZ) domains, with LZ1-3 required for HSF oligomerization. A third HR region (HR-C), which forms LZ4, suppresses HSF activity through intramolecular interactions with LZ1-3 in HSF1 and HSF2. Transcriptional activity for some HSFs requires the activation domain (AD). Sequence similarity was determined using Clustal Omega Multiple Sequence Alignment with protein amino acid sequences obtained from Ensembl. Sequence similarity is scored from 0 to 10, which is indicated by the height and color of the bars under the respective HSF diagrams.

Check out this new review from Roger Smith and Marc Mendillo @feinberg.northwestern.edu on the role of heat shock transcription factors in #development, #NeurodegenerativeDisease and #cancer, and their emerging therapeutic potential

doi.org/10.1242/dmm....

1 week ago 0 0 0 0
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Vaccinology: A New Era in Immune-Driven Vaccine Design | Keystone Symposia Join us at the Keystone Symposia on Vaccinology: A New Era in Immune-Driven Vaccine Design, May 2026, in Killarney, with field leaders!

Our Reviews Editor, Dr Dina Mikimoto, is attending #Vaccinology : A New Era in #VaccineDesign, this May in Killarney with @keystoneSymposia.bsky.social Looking forward to big ideas, bold science, and great conversations. keysym.us/KSVaccines26 #KSVaccines26

1 week ago 1 0 0 0
Figure showing experimental set-up for ototoxicity study, demonstrating that vibratome sectioning preserves otic vesicles. Panel A illustrates vibratome sectioning of day‑75 IEOs into ~200 µm slices, followed by 48 h recovery and 24 h drug treatment at day 77. Sections were fixed were fixed at 1, 3 or 7 days after treatment. (B) Side-view representative image of an IEO sectioned into 200 µm-thick slices. (C) Top-view representation of a vibratome slice of an IEO, with arrowheads annotating the otic vesicles (inset). Scale bars: 100 µm and 500 µm. (D) Intact morphology of an otic vesicle without vibratoming (I), directly after vibratoming (II) and after 48 h recovery (III), showing Hematoxylin and Eosin (H&E) histological staining, followed by immunofluorescent staining of otic epithelium [CDH1+ (green)/SOX10+ (cyan)] and of otic vesicles containing hair cells (MYO7A+, yellow), neurons (TUBB3+, magenta) and cell nuclei (DAPI+, dark blue). In III, the apparent MYO7A–TUBB3 colocalization likely reflects immature hair cell precursors that transiently co-express neuronal β-III-tubulin during development. Scale bars: 25 µm.

Figure showing experimental set-up for ototoxicity study, demonstrating that vibratome sectioning preserves otic vesicles. Panel A illustrates vibratome sectioning of day‑75 IEOs into ~200 µm slices, followed by 48 h recovery and 24 h drug treatment at day 77. Sections were fixed were fixed at 1, 3 or 7 days after treatment. (B) Side-view representative image of an IEO sectioned into 200 µm-thick slices. (C) Top-view representation of a vibratome slice of an IEO, with arrowheads annotating the otic vesicles (inset). Scale bars: 100 µm and 500 µm. (D) Intact morphology of an otic vesicle without vibratoming (I), directly after vibratoming (II) and after 48 h recovery (III), showing Hematoxylin and Eosin (H&E) histological staining, followed by immunofluorescent staining of otic epithelium [CDH1+ (green)/SOX10+ (cyan)] and of otic vesicles containing hair cells (MYO7A+, yellow), neurons (TUBB3+, magenta) and cell nuclei (DAPI+, dark blue). In III, the apparent MYO7A–TUBB3 colocalization likely reflects immature hair cell precursors that transiently co-express neuronal β-III-tubulin during development. Scale bars: 25 µm.

In a new paper in our #InVitroModelling Special Issue, @amylucassen.bsky.social, Heiko Locher & co develop human #iPSC derived inner ear #organoids that reveal ototoxicity in response to cisplatin and gentamicin

doi.org/10.1242/dmm....

2 weeks ago 1 0 0 0

The money question comes up often in conversations with scientists, so our journals chose to address it directly and be transparent about the cost of publishing. Our latest Editorial breaks down exactly where that money goes.

2 weeks ago 2 0 0 0
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Photo of Muhammad Dimas Reza Rahmana

Photo of Muhammad Dimas Reza Rahmana

We interviewed the first author Muhammad Dimas Reza Rahmana

"We believe that publishing in DMM will attract more readers from various backgrounds who are interested in disease modelling and stimulate further research in this field"

Read the full interview here:
doi.org/10.1242/dmm....

2 weeks ago 2 0 0 0
Histological staining and immunofluorescence of the in vitro endometriosis model. Attachment of endometrial (E) to peritoneal (P) constructs is observed after 3 and 10 days of culture (top and bottom row, respectively). The endometrial–peritoneal interface (EPI; dotted line) was composed of cells expressing cytokeratin (CK) and CD10, with some endometrial stromal cells, the CD10-positive cells, appearing to migrate to the peritoneal compartment (arrows). Scale bars: 200 µm; 50 µm (insets).

Histological staining and immunofluorescence of the in vitro endometriosis model. Attachment of endometrial (E) to peritoneal (P) constructs is observed after 3 and 10 days of culture (top and bottom row, respectively). The endometrial–peritoneal interface (EPI; dotted line) was composed of cells expressing cytokeratin (CK) and CD10, with some endometrial stromal cells, the CD10-positive cells, appearing to migrate to the peritoneal compartment (arrows). Scale bars: 200 µm; 50 µm (insets).

In a new Resources & Methods paper in our #InVitroModelling Speical Issue, Rahmana, Hapangama & co develop an in vitro model of peritoneal #endometriosis using patient-derived cells to accelerate understanding of disease onset & development of novel treatment options
doi.org/10.1242/dmm....

2 weeks ago 2 1 1 0
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Cxcr4 – a targetable driver of NF1-behavioral deficits Neurofibromatosis type 1 (NF1) is amongst the most common monogenic neurodevelopmental disorder, affecting ∼1 in 2800 live births worldwide. While most of the research has focused on NF1 as a tumor…

Read the thought-provoking highlight written by expert Dr Corina Anastasaki @washumedicine.bsky.social

"Importantly from a translational medicine lens, this study highlights the potential of repurposing drugs for the treatment of NF1-associated neurocognitive dysfunction"

doi.org/10.1242/dmm....

3 weeks ago 0 0 0 0
Fluorescent microscopy image of nf1 zebrafish model. Green signals represent increased pERK levels in nf1 mutant larvae compared to wild type. Magenta signals denote decreased levels of phosphorylated ERK1/2 (pERK) in nf1 mutant larvae compared to those in wild type.

Fluorescent microscopy image of nf1 zebrafish model. Green signals represent increased pERK levels in nf1 mutant larvae compared to wild type. Magenta signals denote decreased levels of phosphorylated ERK1/2 (pERK) in nf1 mutant larvae compared to those in wild type.

The latest #EditorsChoice is from Miller, Halloran & co @uwmadison.bsky.social as they show that inhibition of chemokine receptor (Cxcr4) signaling improves habituation learning and increases cAMP signaling in a #zebrafish model of neurofibromatosis #NF1

doi.org/10.1242/dmm....

3 weeks ago 0 0 1 1
A promotional graphic for the “4th Metabolism in Health & Disease Conference” on 10–13 October 2026 in Lisbon, Portugal. The theme of the conference is “Understanding the role of metabolism in aging, physiology & disease” and ECR grants of €500 & €1,000 are available. To apply email chloe@fusion-conferences.com with an abstract for a short talk or poster consideration and a summary as to why you would benefit from attending the meeting (further details on website). The abstract submission deadline for talks is 13 April 2026.

A promotional graphic for the “4th Metabolism in Health & Disease Conference” on 10–13 October 2026 in Lisbon, Portugal. The theme of the conference is “Understanding the role of metabolism in aging, physiology & disease” and ECR grants of €500 & €1,000 are available. To apply email chloe@fusion-conferences.com with an abstract for a short talk or poster consideration and a summary as to why you would benefit from attending the meeting (further details on website). The abstract submission deadline for talks is 13 April 2026.

Don't miss the @fusionconf.bsky.social 4th Metabolism in Health & Disease conference.

For all those investigating individual molecules, to those carrying out population studies & clinical trials:

📆Talk submission: 13 April

💰Grants & discounts available

See website for details: bit.ly/4brQTC6

3 weeks ago 1 0 0 0

This Special Issue "#InVitro Models of Human Disease to Inform Mechanism and Drug Discovery" will close in June 2026, so keep an eye out for more articles to come!

journals.biologists.com/dmm/issue/19/6

3 weeks ago 1 0 0 0
Photo of Hans Clevers

Photo of Hans Clevers

Our new Special Issue has launched with a fascinating interview with @hansclevers.bsky.social where he discusses the future of #organoid and #StemCell research

"My personal opinion is that the strength of the organoids is their simplicity."

doi.org/10.1242/dmm....
@hubrechtinstitute.bsky.social

3 weeks ago 2 0 1 0
Images showing qualitative differences in periodic acid–Schiff (PAS) staining intensity (to visualize glycogen deposition) between tissue from WT and transgenic knock-in (KI) mouse carrying the Gaa c.1826dupA variant that is associated with Pompe disease. (A-X) Representative histological images of heart (A-D, M-P), diaphragm (E-H, Q-T) and gastrocnemius tissues (I-L, U-X) at 12 weeks (left) and 72 weeks (right) reveal increased PAS staining intensity in KI mice compared to WT controls. Notable differences in staining intensity are in the heart and gastrocnemius tissues, with more-subtle changes observed in the diaphragm.

Images showing qualitative differences in periodic acid–Schiff (PAS) staining intensity (to visualize glycogen deposition) between tissue from WT and transgenic knock-in (KI) mouse carrying the Gaa c.1826dupA variant that is associated with Pompe disease. (A-X) Representative histological images of heart (A-D, M-P), diaphragm (E-H, Q-T) and gastrocnemius tissues (I-L, U-X) at 12 weeks (left) and 72 weeks (right) reveal increased PAS staining intensity in KI mice compared to WT controls. Notable differences in staining intensity are in the heart and gastrocnemius tissues, with more-subtle changes observed in the diaphragm.

Harb, @WangLysolab & co present a comprehensive natural history of a Pompe disease mouse model - comprising a human-relevant mutation - that recapitulates key disease features and can be used in preclinical therapeutic testing

doi.org/10.1242/dmm....

3 weeks ago 0 0 0 0
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A figure showing the characterisation of larval shape. (A) Schematic of larvae in elongated and bent shapes, then showing the major (a) and minor (b) axis and an ellipse drawn over the larvae to show how they are determined to be in a bent state using ellipses and the major-to-minor axis ratio (R=a/b). (B) A graph of plotted z-scores of R for five larvae in different colours. Example images of larval orientations at different z-scores are overlaid. The cutoff for the ‘bent’ shape was visually determined to be z≥0.8. (C) Output images of larval tracks show darker-coloured tracks when a larva is elongated and a lighter colour when it is bent.

A figure showing the characterisation of larval shape. (A) Schematic of larvae in elongated and bent shapes, then showing the major (a) and minor (b) axis and an ellipse drawn over the larvae to show how they are determined to be in a bent state using ellipses and the major-to-minor axis ratio (R=a/b). (B) A graph of plotted z-scores of R for five larvae in different colours. Example images of larval orientations at different z-scores are overlaid. The cutoff for the ‘bent’ shape was visually determined to be z≥0.8. (C) Output images of larval tracks show darker-coloured tracks when a larva is elongated and a lighter colour when it is bent.

In a new Resources & Methods paper Mele, Johnson & co present an easy-to-use, open-access & customisable tool to analyse #Drosophila larval movements, enabling rapid assessment of organism behaviour without specialised equipment or coding expertise

doi.org/10.1242/dmm....

3 weeks ago 0 0 0 0
Picture of Zolelwa Sifumba

Picture of Zolelwa Sifumba

As today is #WorldTBDay we urge you to read this powerful interview with Dr Zolelwa Sifumba highlighting how her experience as a #tuberculosis survivor, alongside her training as a medical doctor, complements her work as a patient advocate for TBProof in South Africa

doi.org/10.1242/dmm....

4 weeks ago 3 2 0 0
Post image

And here's a quote from the first authors of the paper, Paul and Nirpesh:

"For us, DMM felt like the most natural home for a paper that connects basic developmental biology to a real clinical challenge"

Read an interview with them here:
doi.org/10.1242/dmm....

4 weeks ago 1 0 0 0
Microscopy images showing that transient mesodermal Alx1 expression is essential for extraocular muscle (EOM) myogenesis. Top panels illustrate the transient window of ALX1 expression (magenta) in GFP+ cranial mesoderm at E8.5 (left), followed by its shift to neural crest lineage cells by E9.5 (right). Bottom panels demonstrate that mesoderm-specific Alx1 inactivation leads to the total loss of all seven EOMs (right) by E16.5, compared to the organized EOMs in controls (left; muscle actin is shown in magenta).

Microscopy images showing that transient mesodermal Alx1 expression is essential for extraocular muscle (EOM) myogenesis. Top panels illustrate the transient window of ALX1 expression (magenta) in GFP+ cranial mesoderm at E8.5 (left), followed by its shift to neural crest lineage cells by E9.5 (right). Bottom panels demonstrate that mesoderm-specific Alx1 inactivation leads to the total loss of all seven EOMs (right) by E16.5, compared to the organized EOMs in controls (left; muscle actin is shown in magenta).

This new article from Paul Iyyanar, Nirpesh Adhikari, Yu Lan & Rulang Jiang shows that ALX1 is a crucial transcription factor acting upstream of the gene regulatory network that controls cranial mesoderm patterning and craniofacial #muscledevelopment

doi.org/10.1242/dmm....

4 weeks ago 1 1 1 0
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This Saturday is #IntlForestDay 🌳

DYK that we plant a tree in our forest in the UK for every paper we publish & we preserve a piece of ancient woodland for every peer-reviewer?!

forest.biologists.com

1 month ago 1 0 0 1