Cells & Development

#Question: This may sound like I'm crazy but has anyone experienced immersion oil solidifying or getting stickier after light exposure? Until recently I noticed the oil suddenly gives off a lot of autofluorescence after ~10 mins of imaging, becomes thicker. Have to wipe constantly, really annoying.

#Dros26 Day 2

What antibodies do you wish we had? Comment below your antibody wishlist!

📸 Drosophila egg chamber labeled with DSHB anti-hts in yellow
🧫 dshb.biology.uiowa.edu/hts-RC

Best buddies? More like budding buddies 🪼👯‍♀️✨ Six stages of asexual budding in Hydra to generate new genetically identical individuals (clones). 🟣: collagen 🟢: stem cells. 📸 Image by Ben Cox #FluorescentFriday

Two complementary articles from the lab of Anming Meng and Katie McDole discussing the history and biology of organizer in 🐟, 🐸, and 🐭. Even after more than 100 years since its discovery, major questions remain, especially for mammals.
doi.org/10.1016/j.cd...
doi.org/10.1016/j.cd...

More than 100 years since the discovery of the organiser, there still remains much discussion about the origin, the fate, and the signalling pathways of this important group of cells.

Two complementary articles from the lab of Anming Meng and Katie McDole discussing the history and biology of organizer in 🐟, 🐸, and 🐭. Even after more than 100 years since its discovery, major questions remain, especially for mammals.
doi.org/10.1016/j.cd...
doi.org/10.1016/j.cd...

Data visualization is a critical step in data analysis. 8 links to bookmark for better data visualization:🧵

graphical schematic of the meninges on top depicting the three layers [dura, arachnoid and pia] and other immune and vascular cell types. Inset shows Claudin-11 junction proteins connecting two sides of arachnoid barrier cells bottom schematic is the same but in inflammation with bacteria, junctions breakdown, depiction of cytokine release by vascular, meningeal and immune cells - at side of graphic is summary of defects we observe in infection: 'increased barrier permeability' 'mislocalization of Cldn11+ tight junction' 'BAM activation' and "increased inflammatory response'

🚨 New preprint from our lab led by Sophia Kim w/ @kellydoran.bsky.social group @cuanschutz.bsky.social -- using neonatal 🐭 model of bacterial meningitis ➡️ arachnoid barrier is leaky, Cldn11 junctions are disrupted & cytokines are part of the problem. Lots of 🤩🧠🦠🔬 & compelling data, check it out! 1/5

Valentin Hammoudi, Maria Leptin | EMBO Science Journalism Fellow, former postdoctoral researcher & freelance journalist, talks about their experience with the #fellowship and how they transitioned into #ScienceJournalism: https://www.embo.org/people/bringing-new-perspectives-to-science-journalism/ 🧪

Neurogenesis, as turns out, is highly dependent on cytokine signalings. Even more interesting, the landscape of cytokines in the CNS is highly localised, and a large proportion of cytokine production is done by the meninges. This review by Rua et al discusses in more detail:
doi.org/10.1016/j.cd...

Neurogenesis, as turns out, is highly dependent on cytokine signalings. Even more interesting, the landscape of cytokines in the CNS is highly localised, and a large proportion of cytokine production is done by the meninges. This review by Rua et al discusses in more detail:
doi.org/10.1016/j.cd...

I found this immune cell (🔴) prying open the junction between the ectoderm cells from underneath. You can see its protrusions probing (yellow arrow) and threading through between the other cells before the whole cell body is squeezed through in 1 sweeping motion. So cool! #FluorescenceFriday

Fig. 1. An epigenetic roadmap for early trophoblast development in mice. The trophoblast lineage exhibits lower levels of DNA methylation compared to the embryonic lineage. At the late 2-cell stage, Carm1 expression increases to varying degrees in each blastomere. The high level of Carm1 biases the fate of ICM. As early as the 4-cell stage, all blastomeres initiate an imprinted XCI, which is controlled by maternal H3K27me3 imprinting on the Xist gene. At the 8–16-cell stage, high levels of the chromatin remodeling protein Smarcc1 in partial blastomeres at the late 8-cell stage upregulate epithelial keratins to determine the fate of the trophectoderm. Imprints of placental origin, mediated by the LncRNA Kcnq1ot1, are established during the process of trophoblast lineage differentiation between E4.5 and E7.5. Furthermore, chromatin-modifying enzymes play important roles in post-implantation trophoblast differentiation. ICM, inner cell mass; XCI, chromosome inactivation.

Fig. 4. Chromatin-modifying enzymes and their essential roles in embryonic/fetal development in mice. (A). Null mutations of chromatin-modifying enzymes can lead to embryonic or fetal development failure at various stages. The blue genes are genes that play a role in cell survival. The red genes are genes that play a role in trophoblast development. (B). The phenotypes of placental development defects resulting from mutations in chromatin-modifying enzymes. DNA methylation and histone modifications regulate genomic stability, the imprinting process, chromatin architecture, and gene expression during placental development in mice. Thus, null mutations in essential genes encoding chromatin-modifying enzymes cause various defects in trophoblast development. Kmt5a−/−, Kat5−/−, and Kat8−/− mutations result in cell death. Kdm1a−/−, Nsd1−/−, Prmt1−/−, Prmt5−/−, Ezh2−/−, and Rnf2−/− mutations result in chorion defects. Ehmt2−/− and Dnmt1−/− result in defects in chorioallantoic fusion. Setd2−/− results in defects in vascular branching. me, methylation; ac, acetylation; p, phosphorylation; ub, ubiquitination; dace, deacetylation; dme, demethylation.

The importance of epigenetic modifications in embryonic development has been cemented. In mammals, the trophoblasts play a crucial role in implantation, and their DNA methylation status is crucial. This detailed review by Hua Zhang et al discussed just how important this is:
doi.org/10.1016/j.cd...

I love GFP

✨Kelp embryos looking extra photogenic under the confocal today 🌱🔬 Young Egregia menziesii embryos developing from the megagametophyte 📸 Image by Siobhan Braybrook #FluorescentFriday

An incredibly complicated process and incredibly crucial!

Fig. 1. An epigenetic roadmap for early trophoblast development in mice. The trophoblast lineage exhibits lower levels of DNA methylation compared to the embryonic lineage. At the late 2-cell stage, Carm1 expression increases to varying degrees in each blastomere. The high level of Carm1 biases the fate of ICM. As early as the 4-cell stage, all blastomeres initiate an imprinted XCI, which is controlled by maternal H3K27me3 imprinting on the Xist gene. At the 8–16-cell stage, high levels of the chromatin remodeling protein Smarcc1 in partial blastomeres at the late 8-cell stage upregulate epithelial keratins to determine the fate of the trophectoderm. Imprints of placental origin, mediated by the LncRNA Kcnq1ot1, are established during the process of trophoblast lineage differentiation between E4.5 and E7.5. Furthermore, chromatin-modifying enzymes play important roles in post-implantation trophoblast differentiation. ICM, inner cell mass; XCI, chromosome inactivation.

Fig. 4. Chromatin-modifying enzymes and their essential roles in embryonic/fetal development in mice. (A). Null mutations of chromatin-modifying enzymes can lead to embryonic or fetal development failure at various stages. The blue genes are genes that play a role in cell survival. The red genes are genes that play a role in trophoblast development. (B). The phenotypes of placental development defects resulting from mutations in chromatin-modifying enzymes. DNA methylation and histone modifications regulate genomic stability, the imprinting process, chromatin architecture, and gene expression during placental development in mice. Thus, null mutations in essential genes encoding chromatin-modifying enzymes cause various defects in trophoblast development. Kmt5a−/−, Kat5−/−, and Kat8−/− mutations result in cell death. Kdm1a−/−, Nsd1−/−, Prmt1−/−, Prmt5−/−, Ezh2−/−, and Rnf2−/− mutations result in chorion defects. Ehmt2−/− and Dnmt1−/− result in defects in chorioallantoic fusion. Setd2−/− results in defects in vascular branching. me, methylation; ac, acetylation; p, phosphorylation; ub, ubiquitination; dace, deacetylation; dme, demethylation.

The importance of epigenetic modifications in embryonic development has been cemented. In mammals, the trophoblasts play a crucial role in implantation, and their DNA methylation status is crucial. This detailed review by Hua Zhang et al discussed just how important this is:
doi.org/10.1016/j.cd...

SDB Ethel Browne Harvey Postdoctoral Seminar Series - Gopal Kushawah and Neha Ahuja YouTube video by Society for Developmental Biology

The February 13 #SDBPostdocSeminar with @gopalkushawah.bsky.social of @stowersinstitute.bsky.social and Neha Ahuja of UT Southwestern has been posted. Thank you to moderators Zong-Yuan Liu and @parahsaramore.bsky.social Watch here: youtu.be/aEQuWbfMzWM

Cells moving through tissue interact with the ECM and also with other cells, which can affect morphogenesis. In this interesting paper from the M Lisa Manning lab, Kupffer's Vesicle's trailing cells are shaped by the dragging force from other cells as it moves through tissue.
doi.org/10.1016/j.cd...

Cells moving through tissue interact with the ECM and also with other cells, which can affect morphogenesis. In this interesting paper from the M Lisa Manning lab, Kupffer's Vesicle's trailing cells are shaped by the dragging force from other cells as it moves through tissue.
doi.org/10.1016/j.cd...

A fantastic line up of speakers! Register is now open.

Society for Developmental Biology logo Society for Developmental Biology 2026 Award Winners Edwin G. Conklin Medal Headshot of Lee Niswander Lee Niswander, University of Colorado Boulder Society for Developmental Biology Lifetime Achievement Award Headshot of Alexandra Joyner Alexandra Joyner, Memorial Sloan Kettering Cancer Center Viktor Hamburger Outstanding Educator Prize Headshot of Roberto Mayor Roberto Mayor, University College London Elizabeth D. Hay New Investigator Award Headshot of Jeffrey Farrell Jeffrey Farrell, National Institutes of Health Society for Developmental Biology Trainee Science Communication Award Headshot of Nicholas Desnoyer Nicholas Desnoyer, The Sainsbury Laboratory

Congrats to the 2026 SDB Award Winners!
Conklin Medal: Lee Niswander
SDB Lifetime Achievement Award: Alexandra Joyner
Hamburger Outstanding Educator Prize: Roberto Mayor
Hay New Investigator Award: Jeffrey Farrell
SDB Trainee SciComm Award: Nicholas Desnoyer
bit.ly/4afnjiC

It’s a real honour to receive the Viktor Hamburger Outstanding Educator Prize from the SDB. Teaching is one of the most rewarding parts of my life. Thanks to the SDB and the hundreds of students and faculty at the Quintay course who have made it such a joy.

Fig. 1. What determines the anatomical setpoint of regenerative homeostasis? Planarian flatworms regenerate after amputation using a resident population of stem cells. This process reliably stops when the correct species-specific head shape is restored. The following thought experiment illustrates the profound knowledge gap in our understanding of the rules of morphogenesis despite ample information about genes required for neoblast differentiation. (A) Fragments from a round-head species result in a round-headed regenerate; (B) Fragments from a flat-head species result in flat-headed regenerates. (C) A chimera can be produced by irradiating one species (removing half of the stem cells) and receiving injections of donor neoblasts from a flat-head species. (D) When neoblasts from diverse species combine in the same body, and the head is amputated, what head shape will the regenerative process construct? Despite genomic and molecular-biological information on regeneration in multiple species, the field as yet has no models which make a prediction. This illustrates the importance of chimeras in identifying gaps in our understanding of the rules of emergent processes such as anatomical homeostasis and collective decision-making by cell groups.

✂️ the head of round-head worm => new round head formed.
✂️ the head of flat-head worm => new flat head formed.
What shape will it be if we ✂️ the head of a worm with 50:50 round + flat stem cells?
Check out this exciting review by @drmichaellevin.bsky.social lab!
#chimerism
doi.org/10.1016/j.cd...

Fig. 1. What determines the anatomical setpoint of regenerative homeostasis? Planarian flatworms regenerate after amputation using a resident population of stem cells. This process reliably stops when the correct species-specific head shape is restored. The following thought experiment illustrates the profound knowledge gap in our understanding of the rules of morphogenesis despite ample information about genes required for neoblast differentiation. (A) Fragments from a round-head species result in a round-headed regenerate; (B) Fragments from a flat-head species result in flat-headed regenerates. (C) A chimera can be produced by irradiating one species (removing half of the stem cells) and receiving injections of donor neoblasts from a flat-head species. (D) When neoblasts from diverse species combine in the same body, and the head is amputated, what head shape will the regenerative process construct? Despite genomic and molecular-biological information on regeneration in multiple species, the field as yet has no models which make a prediction. This illustrates the importance of chimeras in identifying gaps in our understanding of the rules of emergent processes such as anatomical homeostasis and collective decision-making by cell groups.

✂️ the head of round-head worm => new round head formed.
✂️ the head of flat-head worm => new flat head formed.
What shape will it be if we ✂️ the head of a worm with 50:50 round + flat stem cells?
Check out this exciting review by @drmichaellevin.bsky.social lab!
#chimerism
doi.org/10.1016/j.cd...

🎇 Calling for paper submission to our Special issue "Tissue Biology – at the interface between immunology and developmental biology". This issue focuses on the interactions between resident immune cells and the surrounding tissue.

Deadline: ‼️30th March 2026‼️

www.sciencedirect.com/special-issu...

Animal caps are the original organoid!

Fig. 1. Animal cap assay and sandwich method as in vitro induction systems. In amphibians, a blastocoel cavity clearly forms inside the animal hemisphere during the blastula and early gastrula stages. The cap-like portion lining the roof of the blastocoel cavity is the animal cap. This region consists of a sheet of pluripotent cells, organized into one or several layers. In the animal cap assay, the animal cap was treated with a physiological saline solution containing inducing factors and then cultured. Depending on the type, concentration, and duration of exposure to the inducing factors, animal caps can differentiate into various cell types. In contrast, the sandwich method, involves culturing the inducer source in between two animal caps. In this technique, the sources of induction can include the dorsal lip of the blastopore (organizer), adult tissues, pelletized soluble factors, or animal caps pretreated with soluble factors. In this figure, activin is used as an example of an inducing factor.

Fig. 12. Summary of the in vitro induction system using activin as an inducing factor. This in vitro induction system utilizes activin and retinoic acid as inducing factors to treat animal caps, employing techniques such as animal cap assay, dissociation/reaggregation protocol, and the sandwich method. By applying these methods, various levels of self-organization can be replicated and controlled in vitro, ranging from lower-order cell differentiation to higher-order tissue differentiation, organogenesis, and even the formation of fundamental body plans. Abbreviations: Dorsal [D], ventral [V], and retinoic acid [RA].

Fig. 11. Formation of embryoids by artificial activin concentration gradients. To create embryoids, animal caps were prepared through treatment with low (0.5–1 ng/ml), intermediate (5–10 ng/ml), or high (50–100 ng/ml) concentrations of activin. These three types of activin-treated animal caps were then sequentially arranged and cultured with untreated animal caps. After 3 days of culture, embryoids with distinct head and trunk-tail structures were formed (A). Histological sections revealed differentiation into head tissues, such as the cement gland [cg] and eyes, and trunk-tail tissues including the ear vesicle [ev], brain [br], notochord [not], muscle [mus], and gut (B). When newt embryos are used in similar combination cultures, neural plate structures forming the brain [white arrow] and axial structures forming the trunk-tail regions [black arrow] are sometimes observed (C).

Fig. 7. In vitro heart formation and in vivo transplantation experiment. When treated with a high concentration of activin, the animal caps of Xenopus embryos did not differentiate into heart tissue. However, if the animal cap dissociates into individual cells before activin treatment and then reaggregates, it forms a beating heart [arrow] with 100 % efficiency (A). This heart expresses differentiation marker genes, such as Nkx2.5, GATA-4, Tbx5, MHCα, TnIc (cardiac troponin I), and ANF, none of which are expressed in an animal cap treated with activin alone, without dissociation/reaggregation (B). Electron microscopy reveals the presence of intercalated discs [id] specific to the cardiac muscle, along with visible mitochondria [m] and Z-bands [z] (C). When the reaggregated heart tissue is orthotopically transplanted into the cardiac primordium of a neurula-stage embryo, it integrates without rejection and continues to beat (D), although it does not persist through host metamorphosis. In contrast, when the reaggregated tissue is ectopically transplanted into the ventral region of the neurula, it begins to beat synchronously with the host heart and gradually reddens as it initiates blood circulation (E).

A fascinating review on the role of Activin in organ induction. Isn't it wild that in Xenopus embryos, a piece of the animal cap can be induced with Activin at different concentrations and buffers to form the ❤️, kidney, the pancreas, head, tail, and even a whole embryoid 🤯:
doi.org/10.1016/j.cd...

A whole embryoid is wild. Check out this review by Makoto Asashima et al.

Fig. 1. Animal cap assay and sandwich method as in vitro induction systems. In amphibians, a blastocoel cavity clearly forms inside the animal hemisphere during the blastula and early gastrula stages. The cap-like portion lining the roof of the blastocoel cavity is the animal cap. This region consists of a sheet of pluripotent cells, organized into one or several layers. In the animal cap assay, the animal cap was treated with a physiological saline solution containing inducing factors and then cultured. Depending on the type, concentration, and duration of exposure to the inducing factors, animal caps can differentiate into various cell types. In contrast, the sandwich method, involves culturing the inducer source in between two animal caps. In this technique, the sources of induction can include the dorsal lip of the blastopore (organizer), adult tissues, pelletized soluble factors, or animal caps pretreated with soluble factors. In this figure, activin is used as an example of an inducing factor.

Fig. 12. Summary of the in vitro induction system using activin as an inducing factor. This in vitro induction system utilizes activin and retinoic acid as inducing factors to treat animal caps, employing techniques such as animal cap assay, dissociation/reaggregation protocol, and the sandwich method. By applying these methods, various levels of self-organization can be replicated and controlled in vitro, ranging from lower-order cell differentiation to higher-order tissue differentiation, organogenesis, and even the formation of fundamental body plans. Abbreviations: Dorsal [D], ventral [V], and retinoic acid [RA].

Fig. 11. Formation of embryoids by artificial activin concentration gradients. To create embryoids, animal caps were prepared through treatment with low (0.5–1 ng/ml), intermediate (5–10 ng/ml), or high (50–100 ng/ml) concentrations of activin. These three types of activin-treated animal caps were then sequentially arranged and cultured with untreated animal caps. After 3 days of culture, embryoids with distinct head and trunk-tail structures were formed (A). Histological sections revealed differentiation into head tissues, such as the cement gland [cg] and eyes, and trunk-tail tissues including the ear vesicle [ev], brain [br], notochord [not], muscle [mus], and gut (B). When newt embryos are used in similar combination cultures, neural plate structures forming the brain [white arrow] and axial structures forming the trunk-tail regions [black arrow] are sometimes observed (C).

Fig. 7. In vitro heart formation and in vivo transplantation experiment. When treated with a high concentration of activin, the animal caps of Xenopus embryos did not differentiate into heart tissue. However, if the animal cap dissociates into individual cells before activin treatment and then reaggregates, it forms a beating heart [arrow] with 100 % efficiency (A). This heart expresses differentiation marker genes, such as Nkx2.5, GATA-4, Tbx5, MHCα, TnIc (cardiac troponin I), and ANF, none of which are expressed in an animal cap treated with activin alone, without dissociation/reaggregation (B). Electron microscopy reveals the presence of intercalated discs [id] specific to the cardiac muscle, along with visible mitochondria [m] and Z-bands [z] (C). When the reaggregated heart tissue is orthotopically transplanted into the cardiac primordium of a neurula-stage embryo, it integrates without rejection and continues to beat (D), although it does not persist through host metamorphosis. In contrast, when the reaggregated tissue is ectopically transplanted into the ventral region of the neurula, it begins to beat synchronously with the host heart and gradually reddens as it initiates blood circulation (E).

A fascinating review on the role of Activin in organ induction. Isn't it wild that in Xenopus embryos, a piece of the animal cap can be induced with Activin at different concentrations and buffers to form the ❤️, kidney, the pancreas, head, tail, and even a whole embryoid 🤯:
doi.org/10.1016/j.cd...