Adam C. Martin
VerifiedMassachusetts Institute of Technology · Biology
Active 1993–2026
About
Adam C. Martin is the Salvador E. Luria Professor and Co-Undergraduate Officer at MIT Department of Biology. He studies molecular mechanisms that underlie tissue form and function, focusing on how cells and tissues change shape during embryonic development. His research visualizes these changes to determine how mechanical forces drive massive tissue movements in the fruit fly, Drosophila melanogaster. Additionally, he investigates the regulation of tissue integrity, specifically examining processes that regulate the epithelial-to-mesenchymal transition (EMT).
Research topics
- Biology
- Cell biology
- Biophysics
- Anatomy
- Physics
Selected publications
2026-02-25
peer-reviewSenior authorBitesize bundles F-actin and influences actin remodeling in syncytial Drosophila embryo development.
PubMed · 2026-07-06
articleSenior authorActin networks undergo rearrangements that influence cell shape. Actin network organization is regulated by a host of actin-binding proteins. The Drosophila synaptotagmin-like protein, bitesize (Btsz), organizes actin at epithelial cell apical junctions in a manner that depends on its interaction with the actin-binding protein, moesin. Using RNAi, we showed that Btsz functions at earlier, syncytial stages of Drosophila embryo development. Btsz is required to stabilize pseudo-cleavage furrows, preventing metaphase spindle collisions and nuclear fallout prior to cellularization. While previous studies have focused on Btsz function through moesin, we find that phosphorylated moesin localized to the nuclear envelope and was not enriched at pseudo-cleavage furrows, suggesting a moesin-independent function for Btsz in syncytial embryos. Consistent with this, mutants that affected all moesin-binding domain isoforms did not recapitulate pan-isoform Btsz depletion and we find that the C-terminal half of Btsz cooperatively binds to and bundles F-actin. We propose that synaptotagmin-like proteins directly regulate actin organization during syncytial Drosophila development.
An actomyosin-mediated mechanical mechanism for brain neural tube elevation
bioRxiv (Cold Spring Harbor Laboratory) · 2025-05-15 · 6 citations
preprintOpen accessSenior authorCorrespondingOrganisms mold their tissues into increasingly more complicated shapes during development using a set of deformation motifs. One set of motifs are tissue hinges and creases which are created through cell-level shape changes. Hinges and creases are often made from active, anisotropic cell constriction at the hinge, which can help drive tissue folding. This contractile hinge model is observed in a variety of developmental tissue folding contexts, like during neural tube closure (NTC) of commonly studied species. However, patterns of cells constriction are inconsistent with this model, in the mouse brain. Additionally, formation of the midline neural tube hinge and crease are insensitive to the molecular machinery needed to induce cell shape changes. Here, we test if a contractile hinge is the driving mechanism for mouse cranial NTC. Through targeted laser ablations, we infer tissue tension in the folding mouse cranial neural tube. In contrast to predications of the contractile hinge model, we find the midline hinge has relatively low and isotropic tension, the lateral neural folds have higher anisotropic tension. We also show that regional patterns of tension vary by sex. We propose a lateral tension model for mouse cranial NTC and theorize on the connection between tissue mechanics and sex in NTC defects.
bioRxiv (Cold Spring Harbor Laboratory) · 2024-02-02 · 1 citations
preprintOpen accessSenior authorCorrespondingAbstract The regulation of the cytoskeleton by multiple pathways, sometimes in parallel, is a common principle of morphogenesis. A classic example of regulation by parallel pathways is Drosophila gastrulation, where the inputs from the Folded gastrulation (Fog)/Concertina (Cta) and the T48 pathways induce apical constriction and mesoderm invagination. Whether there are distinct roles for these separate pathways in regulating the complex spatial and temporal patterns of cytoskeletal activity that accompany early embryo development is still poorly understood. We investigated the roles of the Fog/Cta and T48 pathways and found that, by themselves, the Cta and T48 pathways both promote timely mesoderm invagination and apical myosin II accumulation, with Cta being required for timely cell shape change ahead of mitotic cell division. We also identified distinct functions of T48 and Cta in regulating cellularization and the uniformity of the apical myosin II network, respectively. Our results demonstrate that both redundant and distinct functions for the Fog/Cta and T48 pathways exist.
Proceedings of the National Academy of Sciences · 2024-09-18 · 5 citations
articleOpen accessOvulation is critical for sexual reproduction and consists of the process of liberating fertilizable oocytes from their somatic follicle capsules, also known as follicle rupture. The mechanical force for oocyte expulsion is largely unknown in many species. Our previous work demonstrated that Drosophila ovulation, as in mammals, requires the proteolytic degradation of the posterior follicle wall and follicle rupture to release the mature oocyte from a layer of somatic follicle cells. Here, we identified actomyosin contraction in somatic follicle cells as the major mechanical force for follicle rupture. Filamentous actin (F-actin) and nonmuscle myosin II (NMII) are highly enriched in the cortex of follicle cells upon stimulation with octopamine (OA), a monoamine critical for Drosophila ovulation. Pharmacological disruption of F-actin polymerization prevented follicle rupture without interfering with the follicle wall breakdown. In addition, we demonstrated that OA induces Rho1 guanosine triphosphate (GTP)ase activation in the follicle cell cortex, which activates Ras homolog (Rho) kinase to promote actomyosin contraction and follicle rupture. All these results led us to conclude that OA signaling induces actomyosin cortex enrichment and contractility, which generates the mechanical force for follicle rupture during Drosophila ovulation. Due to the conserved nature of actomyosin contraction, this work could shed light on the mechanical force required for follicle rupture in other species including humans.
Developmental Cell · 2024-10-25 · 8 citations
articleOpen accessSenior authorCorrespondingMorphogenesis: Setting the pace of embryo folding
Current Biology · 2024-04-01
letterOpen accessSenior authorCorrespondingMolecular Biology of the Cell · 2024-03-27 · 5 citations
articleOpen accessSenior authorThe regulation of the cytoskeleton by multiple signaling pathways, sometimes in parallel, is a common principle of morphogenesis. A classic example of regulation by parallel pathways is Drosophila gastrulation, where the inputs from the Folded gastrulation (Fog)/Concertina (Cta) and the T48 pathways induce apical constriction and mesoderm invagination. Whether there are distinct roles for these separate pathways in regulating the complex spatial and temporal patterns of cytoskeletal activity that accompany early embryo development is still poorly understood. We investigated the roles of the Fog/Cta and T48 pathways and found that, by themselves, the Cta and T48 pathways both promote timely mesoderm invagination and apical myosin II accumulation, with Cta being required for timely cell shape change ahead of mitotic cell division. We also identified distinct functions of T48 and Cta in regulating cellularization and the uniformity of the apical myosin II network, respectively. Our results demonstrate that both redundant and distinct functions for the Fog/Cta and T48 pathways exist.
Current Biology · 2024-04-29 · 13 citations
articleOpen accessSenior author2023-06-15
peer-reviewSenior author
Recent grants
NIH · $734k · 2013
NIH · $86k · 2010
Tissue morphogenesis: From signals to forces
NIH · $3.0M · 2022–2026
Investigating Mechanisms of Force Transmission in Tissue Morphogenesis
NIH · $2.4M · 2013–2022
Investigating RhoA GTPase regulation in sculpting tissues
NIH · $1.3M · 2018–2022
Frequent coauthors
- 17 shared
Jörn Dunkel
Massachusetts Institute of Technology
- 13 shared
Soline Chanet
Centre National de la Recherche Scientifique
- 12 shared
Eric Wieschaus
Princeton University
- 12 shared
Jonathan A. Jackson
Massachusetts Institute of Technology
- 11 shared
Matthias Kaschube
Frankfurt Institute for Advanced Studies
- 10 shared
Michael A. Gelbart
University of British Columbia
- 9 shared
Frank M. Mason
Vanderbilt University Medical Center
- 8 shared
Hannah Yevick
Brandeis University
Labs
MIT Department of BiologyPI
Education
- 2006
Ph.D., Molecular and Cell Biology
University of California Berkeley UC Data
- 2000
B.S., Biology
Cornell University
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