🐌 Apple Snail (Pomacea canaliculata). A powerful model for eye regeneration! 👁️Can fully regenerate complex eyes, even after removal. 🌎 Offers insight into how complex organs regenerate #ModelMonday #DevBio #EvoDevo #Regeneration 📸 Image by @accorsi-alice.bsky.social
Calling all microscopy enthusiasts!
Optogenetic mediated contractility enables reversible control of microglial morphology and migration in vivo
It's finally here! Great start of the summer. We got our latest preprint from @chemamd.bsky.social in @qmulsbbs.bsky.social @qmulse.bsky.social, showing evidence of developmental system drift in the specification of dorsoventral (belly vs back) axis in annelids 🪱🪱🪱
#DevBio #EvoDevo
That was meant to say *upregulated, not unregulated.
🪱 Serving head-to-tail fluorescence 💅 Whole-animal FISH in the planaria Schmidtea mediterranea: 🔵 Head 🟣 Gut 🟡 Tail ✨ Masters of regeneration and color coordination 📸 Image from Viraj Doddihal #FluorescenceFriday
To be featured submit your images here ➡️ forms.gle/PWyaViekkNNn...
Fig. 1. Early expression of TgBAC(ankrd1a:EGFP) transgene in the border zone CMs. Hearts of TgBAC(ankrd1a:EGFP);Tg(−0.8myl7:nls-DsRedExpress) (n = 4) were cryoinjured and left to recover for 6 and 15 h. White dashed line outlines the ventricle. Scale bars, 200 μm.
Fig. 6. Persistent TgBAC(ankrd1a:EGFP) expression in CMs adjacent to the residual scar. Hearts (n = 4) of TgBAC(ankrd1a:EGFP);Tg(−0.8myl7:nls-DsRedExpress) zebrafish were cryoinjured and analyzed at 30 dpci, showing different levels of scar resolution (least (A) to most (D) regenerated). The whole hearts after dissection were imaged by fluorescence microscopy (A-D). Serial sections were used for AFOG staining (bright-field images on panels А'-D′) and fluorescence imaging by confocal microscopy (А"-D″). In the indicated region of injury on panels A'-D′, collagen is stained blue, fibrin is stained orange, and CMs are stained brown. Scale bar, 100 μm.
An interesting paper from the Kojic lab shows that ankrd1a - a stress responsive gene is consistently unregulated near damaged site in the ❤️ in zebrafish. Loss of ankrd1a leads to an increase in dedifferentiating cells. Check it out here:
doi.org/10.1016/j.cd...
Amazing opportunity!!
This program transformed my career! Please apply.
@hhmi-science.bsky.social's #FreemanHrabowski Scholars Program offers early career faculty up to $10M over 10 yrs, plus salary & benefits. Postdoc? This year's competition has a program for you too. Applications open 11/3! bit.ly/4vhC0LA
Lovely highlight of a new fascinating study by @ehoffmanlab.bsky.social 🐟💊
For those interested, 🔗 to original research: www.pnas.org/doi/10.1073/...
We love #zebrafish too!
Fig. 1. Early expression of TgBAC(ankrd1a:EGFP) transgene in the border zone CMs. Hearts of TgBAC(ankrd1a:EGFP);Tg(−0.8myl7:nls-DsRedExpress) (n = 4) were cryoinjured and left to recover for 6 and 15 h. White dashed line outlines the ventricle. Scale bars, 200 μm.
Fig. 6. Persistent TgBAC(ankrd1a:EGFP) expression in CMs adjacent to the residual scar. Hearts (n = 4) of TgBAC(ankrd1a:EGFP);Tg(−0.8myl7:nls-DsRedExpress) zebrafish were cryoinjured and analyzed at 30 dpci, showing different levels of scar resolution (least (A) to most (D) regenerated). The whole hearts after dissection were imaged by fluorescence microscopy (A-D). Serial sections were used for AFOG staining (bright-field images on panels А'-D′) and fluorescence imaging by confocal microscopy (А"-D″). In the indicated region of injury on panels A'-D′, collagen is stained blue, fibrin is stained orange, and CMs are stained brown. Scale bar, 100 μm.
An interesting paper from the Kojic lab shows that ankrd1a - a stress responsive gene is consistently unregulated near damaged site in the ❤️ in zebrafish. Loss of ankrd1a leads to an increase in dedifferentiating cells. Check it out here:
doi.org/10.1016/j.cd...
Has this been resolved yet because we're struggling to verify our age. Keep getting error saying "This information is private and is not shared with other users. Error: Load failed" for our associated account. Very frustrating.
Early bird registration deadline is 8th of May 2026!!
Early bird registration deadline is 8th of May 2026!!
🗓️Key dates:
Early-bird deadline – 8 May 2026
Abstract deadline – 12 June 2026
Final registration deadline – 24 July 2026
🎤An amazing line up of speakers and organised by some of your fav dev bio scientist ;)
@wellcometrust.bsky.social @bsdb.bsky.social @biologists.bsky.social
‼️The registration for the Development Journal Meeting 2026 - Human Development: Stem Cells, Models, Embryos is now open. This year marks a collaboration between @dev-journal.bsky.social and the Human Developmental Biology Initiative consortium.
www.biologists.com/meetings/dev...
We want to hear from you. Help us design an inclusive event for everyone by filling in this short form that won't take you more than a few minutes.
‼️Calling all researchers‼️
We are in the process of preparing for the 2029 ISDB conference in India, and we want to hear from you, especially ECRs in the field. Help us design an inclusive and scientifically exciting event by completing this survey by April 13: forms.office.com/e/w1qbNF6KvL
Thank you
Close up of a larval zebrafish gut. In this image, several phagocytes have wrapped themselves along the intestine, and are sending protrusions into the gut. The gut itself is visible as a simple long tube. Individual lips-rich cells are visible in cyan.
It's a rainy Easter and I'm working on draft 22 (😢) of this manuscript, so here's a mental reset #FluorescenceFriday peek at some wonderfully busy magenta-labeled phagocytes crawling along a lipid-rich (in cyan) larval fish intestine.
The #cytoskeleton contributes to abnormal genome-lamina interactions in LMNA-deficient cardiomyocytes. New study from Kaitlyn M. Shen, Parisha P. Shah, Rajan Jain @pennmedicine.bsky.social and colleagues: rupress.org/jcb/article/...
#Chromatin #epigenetics #Disease #lamin #laminopathies
An interesting paper from the lab of Edgar Krötzsch showing the potential contribution of tissue-resident macrophages in the regeneration of punched holes in mouse's ear. Depleting macrophages with clodronate liposomes reduced regeneration and induced cartilage formation.
doi.org/10.1016/j.cd...
Very happy to share this study from our group and colleagues now out in Science!
We found that in zebrafish, before the immune system is mature, gut epithelial cells perform immune functions by producing the cytokine IL-22 to shape the microbiota to promote early life gut function
#Zebrafish #Gut
Be our Associate Editor!! It's fun 💃
Open Call for Associate Editor of our official journal Cells and Development @cellsdev.bsky.social.
Our current group of Associate Editors:
www.sciencedirect.com/science/arti...
Fig. 1. Force impact on embryogenesis and organogenesis. Compelling evidence from published reports demonstrates that fate and differentiation of embryonic stem cells and adult stem cells depend on forces (shear and/or normal stress), substrate elasticity/viscoelasticity, and substrate topography. The observation from cell culture studies that mesenchymal stem cells undergo neurogenesis on soft substrates is consistent with the finding that a stiffness gradient is responsible for axons to change their turning direction caudally towards soft tissues in the developing Xenopus embryonic brain in vivo. Stem-cell based models are useful in understanding role of forces in the development of embryos, which are inaccessible in vivo for mammalian embryos. Blastoid formation via iPSCs is enhanced by 3D culture and substrate mechanics and may depend on endogenous forces (endo-force). Maturation of cardiomyocytes from iPSC differentiation is promoted by mechanical stretching. iPSC, induced pluripotent stem cells. Force is used here generically to represent any type of mechanical loading (force, torque, tensile or compressive stress, shear stress, torque per volume or specific torque) (exogenously or endogenously).
Fig. 2. A mechanobiology model of tumor cell self-renewal and metastasis. Matrix metalloproteinases (MMPs) from the primary tumor site soften the extracellular matrix (ECM) of the tumor microenvironment and break tumor cell dormancy, leading to tumor cell invasion. Stiff (>800 Pa) differentiated tumor cells and soft (<300 Pa) undifferentiated tumor stem cells such as tumor-repopulating cells (Lv et al., 2020) enter blood vessels (intravasation), arrest at narrow vessels, and exit blood vessels (extravasation) to metastasize to distance sites and form micrometastasis. In some cases, soft tumor stem cells proliferate and self-renew within a soft matrix (e.g., bone marrow, brain, lung, and liver) to establish metastatic colonization and grow into macroscopic metastases, or survive and enter dormancy within the stiff matrix, whereas stiff differentiated tumor cells die in the soft or stiff matrix of a different tissue (denoted by an X). In some other cases, when the matrix of tumor microenvironment of metastatic sites becomes inflamed and then softened, soft dormant tumor stem cells will exit dormancy, self-renew, and grow into clinically-detectable macroscopic metastases. Note that this simple model illustrates an element of the Virchow's postulate and highlights softness-based mechanoregulation of cancer progression, which is also regulated by other physical and soluble factors and cells such as tumor-associated fibroblasts and immune cells.
Fig. 3. Cell softness regulates cytotoxic T cell killing of tumor cells. Cytotoxic T cells enter tumor parenchyma, where the T cells use T cell receptor (TCR) to recognize MHC (major histocompatibility complex)-tumor antigenic peptide complex and form the synapse. The activated T cells then release perforin and granzymes to the synapse space where perforin forms pores on the plasma membrane of target tumor cells and allows the entry of granzymes into the cytoplasm, activating caspases 3 and 7 and leading to tumor cell apoptosis. However, drilling pores by perforin is not only a chemical but also a mechanical process. Cell stiffness (>600 Pa) is required for the pore formation by perforin and cell softness impairs perforin pore formation. Thus, soft (<300 Pa) tumor stem cells such as tumor-repopulating cells use their softness to evade T cell cytolysis by impeding perforin pore formation. On the other hand, activated T cells might be very soft, avoiding autolysis. In addition, it is possible that TCR-MHC binding may be equal in the molecular number but the interacting force may be weaker between the soft tumor cell and the immune cell than between the stiff tumor cell and the immune cell; as a result, the released granzyme and perforin from the immune cell may be less, contributing to less killing of the soft tumor cell. Stiff target cells are engulfed more avidly than soft target cells by macrophages, suggesting that this model may be applied to other immune cells.
Some say development is guided by forces. While the role of chemistry in dev bio is undeniable, growing evidence has pointed out the significant contribution of physics too. Chowdhury et al discuss how forces shape normal and cancer stem cells and the clinical applications.
doi.org/10.1016/j.cd...
Fig. 1. Force impact on embryogenesis and organogenesis. Compelling evidence from published reports demonstrates that fate and differentiation of embryonic stem cells and adult stem cells depend on forces (shear and/or normal stress), substrate elasticity/viscoelasticity, and substrate topography. The observation from cell culture studies that mesenchymal stem cells undergo neurogenesis on soft substrates is consistent with the finding that a stiffness gradient is responsible for axons to change their turning direction caudally towards soft tissues in the developing Xenopus embryonic brain in vivo. Stem-cell based models are useful in understanding role of forces in the development of embryos, which are inaccessible in vivo for mammalian embryos. Blastoid formation via iPSCs is enhanced by 3D culture and substrate mechanics and may depend on endogenous forces (endo-force). Maturation of cardiomyocytes from iPSC differentiation is promoted by mechanical stretching. iPSC, induced pluripotent stem cells. Force is used here generically to represent any type of mechanical loading (force, torque, tensile or compressive stress, shear stress, torque per volume or specific torque) (exogenously or endogenously).
Fig. 2. A mechanobiology model of tumor cell self-renewal and metastasis. Matrix metalloproteinases (MMPs) from the primary tumor site soften the extracellular matrix (ECM) of the tumor microenvironment and break tumor cell dormancy, leading to tumor cell invasion. Stiff (>800 Pa) differentiated tumor cells and soft (<300 Pa) undifferentiated tumor stem cells such as tumor-repopulating cells (Lv et al., 2020) enter blood vessels (intravasation), arrest at narrow vessels, and exit blood vessels (extravasation) to metastasize to distance sites and form micrometastasis. In some cases, soft tumor stem cells proliferate and self-renew within a soft matrix (e.g., bone marrow, brain, lung, and liver) to establish metastatic colonization and grow into macroscopic metastases, or survive and enter dormancy within the stiff matrix, whereas stiff differentiated tumor cells die in the soft or stiff matrix of a different tissue (denoted by an X). In some other cases, when the matrix of tumor microenvironment of metastatic sites becomes inflamed and then softened, soft dormant tumor stem cells will exit dormancy, self-renew, and grow into clinically-detectable macroscopic metastases. Note that this simple model illustrates an element of the Virchow's postulate and highlights softness-based mechanoregulation of cancer progression, which is also regulated by other physical and soluble factors and cells such as tumor-associated fibroblasts and immune cells.
Fig. 3. Cell softness regulates cytotoxic T cell killing of tumor cells. Cytotoxic T cells enter tumor parenchyma, where the T cells use T cell receptor (TCR) to recognize MHC (major histocompatibility complex)-tumor antigenic peptide complex and form the synapse. The activated T cells then release perforin and granzymes to the synapse space where perforin forms pores on the plasma membrane of target tumor cells and allows the entry of granzymes into the cytoplasm, activating caspases 3 and 7 and leading to tumor cell apoptosis. However, drilling pores by perforin is not only a chemical but also a mechanical process. Cell stiffness (>600 Pa) is required for the pore formation by perforin and cell softness impairs perforin pore formation. Thus, soft (<300 Pa) tumor stem cells such as tumor-repopulating cells use their softness to evade T cell cytolysis by impeding perforin pore formation. On the other hand, activated T cells might be very soft, avoiding autolysis. In addition, it is possible that TCR-MHC binding may be equal in the molecular number but the interacting force may be weaker between the soft tumor cell and the immune cell than between the stiff tumor cell and the immune cell; as a result, the released granzyme and perforin from the immune cell may be less, contributing to less killing of the soft tumor cell. Stiff target cells are engulfed more avidly than soft target cells by macrophages, suggesting that this model may be applied to other immune cells.
Some say development is guided by forces. While the role of chemistry in dev bio is undeniable, growing evidence has pointed out the significant contribution of physics too. Chowdhury et al discuss how forces shape normal and cancer stem cells and the clinical applications.
doi.org/10.1016/j.cd...
Looking at you @biologists.bsky.social, @dmmjournal.bsky.social, @plos.org, @elife.bsky.social, @viewpointbehavior.bsky.social, @cp-cellreports.bsky.social, @bionomous.bsky.social, @addgene.bsky.social, @cellsdev.bsky.social, @cancerresearchuk.org, @wellcometrust.bsky.social, @ukri.org 😊 🙏
A movie from 9 years ago and I've never noticed the actin wave inside these cells until now 😱 It looks like a cluster of actin filament moving from 1 place to the other and pushing the cell membrane out to form protrusions. Reminds me of an ocean undercurrent. How interesting! #FluorescenceFriday
Fig. 1. Basic steps of cell migration. (a) Mesenchymal cell migration. Cells are attached to the extracellular matrix (ECM) via integrins and focal adhesions (FA). Actin polymerization at the leading edge extends filamentous actin (F-actin) protrusions inducing a front-rear polarization. New FA adhesions attach the protrusions to the ECM followed by F-actin rearward movement, known as actin retrograde flow. Disassembly of rear FA and myosin II contraction at the back of cell generate the pushing force to move the cell forward. (b) Amoeboid cell migration. Cells do not form adhesions with the ECM or other cells. Under confinement, amoeboid cells form membrane blebs, also known as pseudopodia, inducing a front-rear polarization. Actin retrograde flow is initiated by mechanical forces, such as confinement. Myosin II contraction at the back of cell generates the pushing force to move the cell forward.
Fig. 2. MS ion channel families involved in cell migration. (a) Transient receptor potential channels (TRP). TRP channels form 6 transmembrane (TM) domains. TM 1-2 are represented in cyan, TM 3-4 in orange and TM 5-6 in magenta. The pore forming domain is formed between TM5 and TM6. Each subfamily of TRP channels contains unique domains in the cytoplasmic N- and C- termini. TRPC channels have three ankyrin repeats and a coiled-coil domain in the N-terminus. A TRP domain, which has gating functions, a calmodulin and IP3R binding domains are localized in the C-terminus. TRPV channels have six ankyrin repeats in the N-terminus. A TRP domain, a calmodulin and PIP2 binding domains are localized in the C-terminus. (b–b′) Piezo1 channels. (b) Each Piezo1 channel has at least 26 TM regions and up to 40 TM domains. The TM domains form three defined structures, known as blades. Each blade is colour coded in cyan, orange and magenta for easier representation. The carboy-terminal extracellular domain (CED) is located directly on top of the pore forming domain and is important for ion selectivity (Zhao et al., 2016). (b′) Due to its large size, a Piezo1 channel induces a small curvature to the plasma membrane, when force is applied the plasma membrane is stretched, thereby opening the Piezo1 channel.
Fig. 3. Role of MS ion channels in cell migration. (a) Actin protrusions. MS ion channels can regulate the extension of actin-based protrusions through PI3K signalling. Ca2+ binding to PI3K leads to the activation of several Rac1-GEFs, including P-Rex1 and SWAP-70, Vav1, Sos1. Rac1-GEFs mediate the transition from inactive Rac1-GDP to Rac1-GTP, leading to actin polymerization and protrusion extension. (b) RhoA activation. The Ca2+ sensitive Pyk2 kinase is activated after MS ion channel opening. Pyk2 activates PDZ-RhoGEF which mediates the transition from inactive Rho-GDP to Rho-GTP, leading to Myosin II phosphorylation. Global Myosin II contraction leads to inhibition of cell migration. (c) Chemotaxis. The presence of a chemoattractant agent leads to re-localization of TRPC1 and TRPC6 MS ion channels to the direction of the chemoattractant signal. Localized Ca2+ can regulate actin remodelling via PI3K or induce Ca2+ flickers at the leading edge of the cell, promoting directional cell migration. (d) Focal adhesion (FA) disassembly. MS ion channels regulate FA disassembly via calpain, a Ca2+ dependant protease that mediates FA degradation. Restricted calpain activity at the rear of the cell mediates specific FA disassembly at the back of the cell, promoting cell migration. (e) Yap/Taz nuclear localization. Piezo1 activation is correlated with Yap translocation from the cytoplasm to the nucleus, leading to Yap mediated gene transcription. However, the biochemical signals downstream of Piezo1 have not been identified yet. Dashed line represents unknown signalling proteins.
Many ion channels eg. TRP, Piezo are mechanically sensitive, meaning they can be activated/deactivated by mechanical stimuli such as membrane curvature or substrate stiffness. In this thorough review from the Mayor lab, they discuss how these channels regulate cell migration.
doi.org/10.1016/j.cd...
