Journal articles: 'Tissue folding'

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Zečić, Aleksandra, and Chadanat Noonin. "Whole-mount in situ hybridization: minimizing the folding problem of thin-sheet tissue-like crayfish haematopoietic tissue." Crustaceana 91, no. 1 (2018): 1–15. http://dx.doi.org/10.1163/15685403-00003745.

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Crayfish haematopoietic tissue (HPT) has a thin-sheet-like structure with a thickness of 100-160 μm and a width of approximately 1-2 cm. This structure makes HPT extremely easy to fold after removal from the animal. Therefore, it is difficult to handle the tissue without folding when processing for sectioning and histological study. The degree of tissue folding reflects the size of the tissue sections obtained, how complicated it is to interpret the location of each tissue section, and the accuracy of the interpretation of the location of a specific transcript. To facilitate the interpretation of a specific transcript location in the HPT, we optimized a whole-mount in situ hybridization technique to minimize tissue folding. This optimized protocol effectively reduced the tissue folding. Therefore, the location of a specific transcript in the HPT was easily and accurately defined. This protocol will be useful for whole-mount staining of other tissues with similar structure.

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Inoue, Yasuhiro, Itsuki Tateo, and Taiji Adachi. "Epithelial tissue folding pattern in confined geometry." Biomechanics and Modeling in Mechanobiology 19, no. 3 (November 14, 2019): 815–22. http://dx.doi.org/10.1007/s10237-019-01249-8.

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AbstractThe primordium of the exoskeleton of an insect is epithelial tissue with characteristic patterns of folds. As the insect develops from larva to pupa, the spreading of these folds produces the three-dimensional shape of the exoskeleton of the insect. It is known that the three-dimensional exoskeleton shape has already been encoded in characteristic patterns of folds in the primordium; however, a description of how the epithelial tissue forms with the characteristic patterns of folds remains elusive. The present paper suggests a possible mechanism for the formation of the folding pattern. During the primordium development, because of the epithelial tissue is surrounded by other tissues, cell proliferation proceeds within a confined geometry. To elucidate the mechanics of the folding of the epithelial tissue in the confined geometry, we employ a three-dimensional vertex model that expresses tissue deformations based on cell mechanical behaviors and apply the model to examine the effects of cell divisions and the confined geometry on epithelial folding. Our simulation results suggest that the orientation of the axis of cell division is sufficient to cause different folding patterns in silico and that the restraint of out-of-plane deformation due to the confined geometry determines the interspacing of the folds.

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Hookway, Tracy A. "Engineering Biology by Controlling Tissue Folding." Trends in Biotechnology 36, no. 4 (April 2018): 341–43. http://dx.doi.org/10.1016/j.tibtech.2018.02.003.

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Allen, Simon, Hassan Y. Naim, and Neil J. Bulleid. "Intracellular Folding of Tissue-type Plasminogen Activator." Journal of Biological Chemistry 270, no. 9 (March 3, 1995): 4797–804. http://dx.doi.org/10.1074/jbc.270.9.4797.

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Zartman, Jeremiah J., and Stanislav Y. Shvartsman. "Unit Operations of Tissue Development: Epithelial Folding." Annual Review of Chemical and Biomolecular Engineering 1, no. 1 (June 15, 2010): 231–46. http://dx.doi.org/10.1146/annurev-chembioeng-073009-100919.

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Hiraiwa, Tetsuya, Fu-Lai Wen, Tatsuo Shibata, and Erina Kuranaga. "Mathematical Modeling of Tissue Folding and Asymmetric Tissue Flow during Epithelial Morphogenesis." Symmetry 11, no. 1 (January 19, 2019): 113. http://dx.doi.org/10.3390/sym11010113.

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Recent studies have revealed that intrinsic, individual cell behavior can provide the driving force for deforming a two-dimensional cell sheet to a three-dimensional tissue without the need for external regulatory elements. However, whether intrinsic, individual cell behavior could actually generate the force to induce tissue deformation was unclear, because there was no experimental method with which to verify it in vivo. In such cases, mathematical modeling can be effective for verifying whether a locally generated force can propagate through an entire tissue and induce deformation. Moreover, the mathematical model sometimes provides potential mechanistic insight beyond the information obtained from biological experimental results. Here, we present two examples of modeling tissue morphogenesis driven by cell deformation or cell interaction. In the first example, a mathematical study on tissue-autonomous folding based on a two-dimensional vertex model revealed that active modulations of cell mechanics along the basal–lateral surface, in addition to the apical side, can induce tissue-fold formation. In the second example, by applying a two-dimensional vertex model in an apical plane, a novel mechanism of tissue flow caused by asymmetric cell interactions was discovered, which explained the mechanics behind the collective cellular movement observed during epithelial morphogenesis.

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Chan, Hon Fai, Ruike Zhao, German A. Parada, Hu Meng, Kam W. Leong, Linda G. Griffith, and Xuanhe Zhao. "Folding artificial mucosa with cell-laden hydrogels guided by mechanics models." Proceedings of the National Academy of Sciences 115, no. 29 (July 2, 2018): 7503–8. http://dx.doi.org/10.1073/pnas.1802361115.

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The surfaces of many hollow or tubular tissues/organs in our respiratory, gastrointestinal, and urogenital tracts are covered by mucosa with folded patterns. The patterns are induced by mechanical instability of the mucosa under compression due to constrained growth. Recapitulating this folding process in vitro will facilitate the understanding and engineering of mucosa in various tissues/organs. However, scant attention has been paid to address the challenge of reproducing mucosal folding. Here we mimic the mucosal folding process using a cell-laden hydrogel film attached to a prestretched tough-hydrogel substrate. The cell-laden hydrogel constitutes a human epithelial cell lining on stromal component to recapitulate the physiological feature of a mucosa. Relaxation of the prestretched tough-hydrogel substrate applies compressive strains on the cell-laden hydrogel film, which undergoes mechanical instability and evolves into morphological patterns. We predict the conditions for mucosal folding as well as the morphology of and strain in the folded artificial mucosa using a combination of theory and simulation. The work not only provides a simple method to fold artificial mucosa but also demonstrates a paradigm in tissue engineering via harnessing mechanical instabilities guided by quantitative mechanics models.

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Ko, Clint S., Vardges Tserunyan, and Adam C. Martin. "Microtubules promote intercellular contractile force transmission during tissue folding." Journal of Cell Biology 218, no. 8 (June 21, 2019): 2726–42. http://dx.doi.org/10.1083/jcb.201902011.

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During development, forces transmitted between cells are critical for sculpting epithelial tissues. Actomyosin contractility in the middle of the cell apex (medioapical) can change cell shape (e.g., apical constriction) but can also result in force transmission between cells via attachments to adherens junctions. How actomyosin networks maintain attachments to adherens junctions under tension is poorly understood. Here, we discovered that microtubules promote actomyosin intercellular attachments in epithelia during Drosophila melanogaster mesoderm invagination. First, we used live imaging to show a novel arrangement of the microtubule cytoskeleton during apical constriction: medioapical Patronin (CAMSAP) foci formed by actomyosin contraction organized an apical noncentrosomal microtubule network. Microtubules were required for mesoderm invagination but were not necessary for initiating apical contractility or adherens junction assembly. Instead, microtubules promoted connections between medioapical actomyosin and adherens junctions. These results delineate a role for coordination between actin and microtubule cytoskeletal systems in intercellular force transmission during tissue morphogenesis.

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Codd, S. L., R. K. Lambert, M. R. Alley, and R. J. Pack. "Tensile stiffness of ovine tracheal wall." Journal of Applied Physiology 76, no. 6 (June 1, 1994): 2627–35. http://dx.doi.org/10.1152/jappl.1994.76.6.2627.

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The epithelial folding that occurs during bronchoconstriction requires that the pressure on the muscle side of the folding membrane be greater than that on the lumen side. The pressure required for a given level of folding depends on the elastic properties of the tissue and on the geometry of the folding. To quantify the elastic properties, uniaxial tensile stiffness of the tracheal inner wall of nine sheep was measured in two directions: parallel to the tracheal axis and circumferentially. The tissue showed anisotropic behavior, being approximately three times stiffer longitudinally than circumferentially. Histological examination showed that collagen in the lamina propria was randomly arranged, whereas there were straight elastin fibers aligned with the tracheal axis. This observation could explain the observed elastic anisotropy. Mechanical removal of the epithelium had no effect on tensile stiffness. It was also found that the tissue was under tension in situ. When a strip was excised, its length decreased by > or = 30%. After allowing for the systematic errors inherent in this experiment, the in situ circumferential tensile stiffness is estimated to be > or = 20 kPa. If the equivalent tissue in the bronchioles has the same tensile stiffness as that in the trachea, the forces required to fold the membrane are significant at small transbronchial pressure differences and increase in the presence of membrane thickening such as that seen in asthma.

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Tozluoǧlu, Melda, and Yanlan Mao. "On folding morphogenesis, a mechanical problem." Philosophical Transactions of the Royal Society B: Biological Sciences 375, no. 1809 (August 24, 2020): 20190564. http://dx.doi.org/10.1098/rstb.2019.0564.

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Tissue folding is a fundamental process that sculpts a simple flat epithelium into a complex three-dimensional organ structure. Whether it is the folding of the brain, or the looping of the gut, it has become clear that to generate an invagination or a fold of any form, mechanical asymmetries must exist in the epithelium. These mechanical asymmetries can be generated locally, involving just the invaginating cells and their immediate neighbours, or on a more global tissue-wide scale. Here, we review the different mechanical mechanisms that epithelia have adopted to generate folds, and how the use of precisely defined mathematical models has helped decipher which mechanisms are the key driving forces in different epithelia. This article is part of a discussion meeting issue ‘Contemporary morphogenesis'.

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Mason, Frank M., Shicong Xie, Claudia G. Vasquez, Michael Tworoger, and Adam C. Martin. "RhoA GTPase inhibition organizes contraction during epithelial morphogenesis." Journal of Cell Biology 214, no. 5 (August 22, 2016): 603–17. http://dx.doi.org/10.1083/jcb.201603077.

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During morphogenesis, contraction of the actomyosin cytoskeleton within individual cells drives cell shape changes that fold tissues. Coordination of cytoskeletal contractility is mediated by regulating RhoA GTPase activity. Guanine nucleotide exchange factors (GEFs) activate and GTPase-activating proteins (GAPs) inhibit RhoA activity. Most studies of tissue folding, including apical constriction, have focused on how RhoA is activated by GEFs to promote cell contractility, with little investigation as to how GAPs may be important. Here, we identify a critical role for a RhoA GAP, Cumberland GAP (C-GAP), which coordinates with a RhoA GEF, RhoGEF2, to organize spatiotemporal contractility during Drosophila melanogaster apical constriction. C-GAP spatially restricts RhoA pathway activity to a central position in the apical cortex. RhoGEF2 pulses precede myosin, and C-GAP is required for pulsation, suggesting that contractile pulses result from RhoA activity cycling. Finally, C-GAP expression level influences the transition from reversible to irreversible cell shape change, which defines the onset of tissue shape change. Our data demonstrate that RhoA activity cycling and modulating the ratio of RhoGEF2 to C-GAP are required for tissue folding.

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Johnson, Travis K., Karyn A. Moore, James C. Whisstock, and Coral G. Warr. "Maternal Torso-Like Coordinates Tissue Folding During Drosophila Gastrulation." Genetics 206, no. 3 (May 11, 2017): 1459–68. http://dx.doi.org/10.1534/genetics.117.200576.

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Heer, Natalie C., Pearson W. Miller, Soline Chanet, Norbert Stoop, Jörn Dunkel, and Adam C. Martin. "Actomyosin-based tissue folding requires a multicellular myosin gradient." Journal of Cell Science 130, no. 11 (June 1, 2017): e1.2-e1.2. http://dx.doi.org/10.1242/jcs.206243.

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Gracia, Mélanie, Corinne Benassayag, and Magali Suzanne. "Is Epithelio-Mesenchymal transition actively involved in tissue folding?" Mechanisms of Development 145 (July 2017): S98. http://dx.doi.org/10.1016/j.mod.2017.04.253.

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Hughes, Alex J., Hikaru Miyazaki, Maxwell C. Coyle, Jesse Zhang, Matthew T. Laurie, Daniel Chu, Zuzana Vavrušová, Richard A. Schneider, Ophir D. Klein, and Zev J. Gartner. "Engineered Tissue Folding by Mechanical Compaction of the Mesenchyme." Developmental Cell 44, no. 2 (January 2018): 165–78. http://dx.doi.org/10.1016/j.devcel.2017.12.004.

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Heer, Natalie C., Pearson W. Miller, Soline Chanet, Norbert Stoop, Jörn Dunkel, and Adam C. Martin. "Actomyosin-based tissue folding requires a multicellular myosin gradient." Development 144, no. 10 (April 21, 2017): 1876–86. http://dx.doi.org/10.1242/dev.146761.

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Byers, Peter H. "Folding defects in fibrillar collagens." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 356, no. 1406 (February 28, 2001): 151–58. http://dx.doi.org/10.1098/rstb.2000.0760.

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Fibrillar collagens have a long triple helix in which glycine is in every third position for more than 1000 amino acids. The three chains of these molecules are assembled with specificity into several different molecules that have tissue–specific distribution. Mutations that alter folding of either the carboxy–terminal globular peptides that direct chain association, or of the regions of the triple helix that are important for nucleation, or of the bulk of the triple helix, all result in identifiable genetic disorders in which the phenotype reflects the region of expression of the genes and their tissue–specific distribution. Mutations that result in changed amino–acid sequences in any of these regions have different effects on folding and may have different phenotypic outcomes. Substitution for glycine residues in the triple helical domains are among the most common effects of mutations, and the nature of the substituting residue and its location in the chain contribute to the effect on folding and also on the phenotype. More complex mutations, such as deletions or insertions of triple helix, also affect folding, probably because of alterations in helical pitch along the triple helix. These mutations all interfere with the ability of these molecules to form the characteristic fibrillar array in the extracellular matrix and many result in intracellular retention of abnormal molecules.

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Braakman, I., H. Hoover-Litty, K. R. Wagner, and A. Helenius. "Folding of influenza hemagglutinin in the endoplasmic reticulum." Journal of Cell Biology 114, no. 3 (August 1, 1991): 401–11. http://dx.doi.org/10.1083/jcb.114.3.401.

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The folding of influenza hemagglutinin (HA0) in the ER was analyzed in tissue culture cells by following the formation of intrachain disulfides after short (1 min) radioactive pulses. While some disulfide bonds were already formed on the nascent chains, the subunits acquired their final disulfide composition and antigenic epitopes posttranslationally. Two posttranslational folding intermediates were identified. In CHO cells constitutively expressing HA0, mature HA0 subunits were formed with a half time of 3 min and their folding reached completion at 22 min. The rate of folding was highly dependent on cell type and expression system, and thus regulated by factors other than the sequence of the protein alone. Exposure of cells to stress conditions increased the level of glucose regulated proteins, including BiP, and decreased the folding rate. The efficiency of folding and subsequent trimerization was not dependent on the rate of translation, nor on temperature between 37 and 15 degrees C; however, the rates of folding and trimerization decreased with decreasing temperature. Whereas the rate of folding was independent of expression level, trimerization was accelerated at higher levels of expression.

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Grigoryev, Sergei A. "Higher-order folding of heterochromatin: Protein bridges span the nucleosome arrays." Biochemistry and Cell Biology 79, no. 3 (June 1, 2001): 227–41. http://dx.doi.org/10.1139/o01-030.

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In interphase eukaryotic nuclei, chromatin is divided into two morphologically distinct types known as heterochromatin and euchromatin. It has been long suggested that the two types of chromatin differ at the level of higher-order folding. Recent studies have revealed the features of chromatin 3D architecture that distinguish the higher-order folding of repressed and active chromatin and have identified chromosomal proteins and their modifications associated with these structural transitions. This review discusses the molecular and structural determinants of chromatin higher-order folding in relation to mechanism(s) of heterochromatin formation and genetic silencing during cell differentiation and tissue development.Key words: heterochromatin, nucleosome, histone, higher-order folding, chromatin 3D structure.

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Yoshino, Kunihiko, Kohei Abe, Koyu Suzuki, Rihito Tamaki, Atusyuki Mituishi, Manabu Yamasaki, and Hiroyasu Misumi. "A Novel Technique of Endoscopic Vein Harvesting With Preserved Perivascular Tissue." Innovations: Technology and Techniques in Cardiothoracic and Vascular Surgery 15, no. 5 (September 2020): 475–77. http://dx.doi.org/10.1177/1556984520948139.

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The no-touch saphenous vein harvesting technique is considered to be the ideal procedure to achieve the best quality of vein, whereas the endoscopic vein harvesting (EVH) technique is considered to be ideal for decreasing wound complications. We developed a new technique of EVH with perivascular tissue preservation. This procedure was performed by dissecting the immediate anterior and posterior perivascular connective tissues of the saphenous vein followed by cutting approximately 1 cm laterally from the saphenous vein with the use of a harvester (MAQUET Getinge Group, Getinge AB, Göteborg, Sweden). Histopathological examination revealed preserved perivascular tissue and intimal folding.

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Yevick, Hannah G., Pearson W. Miller, Jörn Dunkel, and Adam C. Martin. "Structural Redundancy in Supracellular Actomyosin Networks Enables Robust Tissue Folding." Developmental Cell 50, no. 5 (September 2019): 586–98. http://dx.doi.org/10.1016/j.devcel.2019.06.015.

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Del-Valle-Anton, Lucia, and Víctor Borrell. "Folding brains: from development to disease modeling." Physiological Reviews 102, no. 2 (April 1, 2022): 511–50. http://dx.doi.org/10.1152/physrev.00016.2021.

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The human brain is characterized by the large size and intricate folding of its cerebral cortex, which are fundamental for our higher cognitive function and frequently altered in pathological dysfunction. Cortex folding is not unique to humans, nor even to primates, but is common across mammals. Cortical growth and folding are the result of complex developmental processes that involve neural stem and progenitor cells and their cellular lineages, the migration and differentiation of neurons, and the genetic programs that regulate and fine-tune these processes. All these factors combined generate mechanical stress and strain on the developing neural tissue, which ultimately drives orderly cortical deformation and folding. In this review we examine and summarize the current knowledge on the molecular, cellular, histogenic, and mechanical mechanisms that are involved in and influence folding of the cerebral cortex, and how they emerged and changed during mammalian evolution. We discuss the main types of pathological malformations of human cortex folding, their specific developmental origin, and how investigating their genetic causes has illuminated our understanding of key events involved. We close our review by presenting the animal and in vitro models of cortex folding that are currently used to study these devastating developmental brain disorders in children, and what are the main challenges that remain ahead of us to fully understand brain folding.

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Kim, Jae-Young, Elizabeth A. Fogarty, Franklin J. Lu, Hui Zhu, Geoffrey D. Wheelock, Lee A. Henderson, and Matthew P. DeLisa. "Twin-Arginine Translocation of Active Human Tissue Plasminogen Activator in Escherichia coli." Applied and Environmental Microbiology 71, no. 12 (December 2005): 8451–59. http://dx.doi.org/10.1128/aem.71.12.8451-8459.2005.

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ABSTRACT When eukaryotic proteins with multiple disulfide bonds are expressed at high levels in Escherichia coli, the efficiency of thiol oxidation and isomerization is typically not sufficient to yield soluble products with native structures. Even when such proteins are secreted into the oxidizing periplasm or expressed in the cytoplasm of cells carrying mutations in the major intracellular disulfide bond reduction systems (e.g., trxB gor mutants), correct folding can be problematic unless a folding modulator is simultaneously coexpressed. In the present study we explored whether the bacterial twin-arginine translocation (Tat) pathway could serve as an alternative expression system for obtaining appreciable levels of recombinant proteins which exhibit complex patterns of disulfide bond formation, such as full-length human tissue plasminogen activator (tPA) (17 disulfides) and a truncated but enzymatically active version of tPA containing nine disulfides (vtPA). Remarkably, targeting of both tPA and vtPA to the Tat pathway resulted in active protein in the periplasmic space. We show here that export by the Tat translocator is dependent upon oxidative protein folding in the cytoplasm of trxB gor cells prior to transport. Whereas previous efforts to produce high levels of active tPA or vtPA in E. coli required coexpression of the disulfide bond isomerase DsbC, we observed that Tat-targeted vtPA and tPA reach a native conformation without thiol-disulfide oxidoreductase coexpression. These results demonstrate that the Tat system may have inherent and unexpected benefits compared with existing expression strategies, making it a viable alternative for biotechnology applications that hinge on protein expression and secretion.

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John, Alphy, and Matteo Rauzi. "A two-tier junctional mechanism drives simultaneous tissue folding and extension." Developmental Cell 56, no. 10 (May 2021): 1469–83. http://dx.doi.org/10.1016/j.devcel.2021.04.003.

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Jung, Sae-Young, Dae-Young Kang, Hyun-Seung Shin, and Jung-Chul Park. "3D analysis of soft tissue around implant after flap folding suture." Journal of Dental Rehabilitation and Applied Science 37, no. 3 (September 30, 2021): 130–37. http://dx.doi.org/10.14368/jdras.2021.37.3.130.

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Visetsouk, Mike R., Elizabeth J. Falat, Ryan J. Garde, Jennifer L. Wendlick, and Jennifer H. Gutzman. "Basal epithelial tissue folding is mediated by differential regulation of microtubules." Development 145, no. 22 (October 17, 2018): dev167031. http://dx.doi.org/10.1242/dev.167031.

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Kim, Hosung, Benoit Caldairou, Ji-Wook Hwang, Tommaso Mansi, Seok-Jun Hong, Neda Bernasconi, and Andrea Bernasconi. "Accurate cortical tissue classification on MRI by modeling cortical folding patterns." Human Brain Mapping 36, no. 9 (June 3, 2015): 3563–74. http://dx.doi.org/10.1002/hbm.22862.

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Sala, Ambre J., Laura C. Bott, and Richard I. Morimoto. "Shaping proteostasis at the cellular, tissue, and organismal level." Journal of Cell Biology 216, no. 5 (April 11, 2017): 1231–41. http://dx.doi.org/10.1083/jcb.201612111.

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The proteostasis network (PN) regulates protein synthesis, folding, transport, and degradation to maintain proteome integrity and limit the accumulation of protein aggregates, a hallmark of aging and degenerative diseases. In multicellular organisms, the PN is regulated at the cellular, tissue, and systemic level to ensure organismal health and longevity. Here we review these three layers of PN regulation and examine how they collectively maintain cellular homeostasis, achieve cell type-specific proteomes, and coordinate proteostasis across tissues. A precise understanding of these layers of control has important implications for organismal health and could offer new therapeutic approaches for neurodegenerative diseases and other chronic disorders related to PN dysfunction.

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Jodoin, Jeanne N., and Adam C. Martin. "Abl suppresses cell extrusion and intercalation during epithelium folding." Molecular Biology of the Cell 27, no. 18 (September 15, 2016): 2822–32. http://dx.doi.org/10.1091/mbc.e16-05-0336.

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Tissue morphogenesis requires control over cell shape changes and rearrangements. In the Drosophila mesoderm, linked epithelial cells apically constrict, without cell extrusion or intercalation, to fold the epithelium into a tube that will then undergo epithelial-to-mesenchymal transition (EMT). Apical constriction drives tissue folding or cell extrusion in different contexts, but the mechanisms that dictate the specific outcomes are poorly understood. Using live imaging, we found that Abelson (Abl) tyrosine kinase depletion causes apically constricting cells to undergo aberrant basal cell extrusion and cell intercalation. abl depletion disrupted apical–basal polarity and adherens junction organization in mesoderm cells, suggesting that extruding cells undergo premature EMT. The polarity loss was associated with abnormal basolateral contractile actomyosin and Enabled (Ena) accumulation. Depletion of the Abl effector Enabled (Ena) in abl-depleted embryos suppressed the abl phenotype, consistent with cell extrusion resulting from misregulated ena. Our work provides new insight into how Abl loss and Ena misregulation promote cell extrusion and EMT.

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Martin, Adam C. "The Physical Mechanisms of Drosophila Gastrulation: Mesoderm and Endoderm Invagination." Genetics 214, no. 3 (March 2020): 543–60. http://dx.doi.org/10.1534/genetics.119.301292.

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A critical juncture in early development is the partitioning of cells that will adopt different fates into three germ layers: the ectoderm, the mesoderm, and the endoderm. This step is achieved through the internalization of specified cells from the outermost surface layer, through a process called gastrulation. In Drosophila, gastrulation is achieved through cell shape changes (i.e., apical constriction) that change tissue curvature and lead to the folding of a surface epithelium. Folding of embryonic tissue results in mesoderm and endoderm invagination, not as individual cells, but as collective tissue units. The tractability of Drosophila as a model system is best exemplified by how much we know about Drosophila gastrulation, from the signals that pattern the embryo to the molecular components that generate force, and how these components are organized to promote cell and tissue shape changes. For mesoderm invagination, graded signaling by the morphogen, Spätzle, sets up a gradient in transcriptional activity that leads to the expression of a secreted ligand (Folded gastrulation) and a transmembrane protein (T48). Together with the GPCR Mist, which is expressed in the mesoderm, and the GPCR Smog, which is expressed uniformly, these signals activate heterotrimeric G-protein and small Rho-family G-protein signaling to promote apical contractility and changes in cell and tissue shape. A notable feature of this signaling pathway is its intricate organization in both space and time. At the cellular level, signaling components and the cytoskeleton exhibit striking polarity, not only along the apical–basal cell axis, but also within the apical domain. Furthermore, gene expression controls a highly choreographed chain of events, the dynamics of which are critical for primordium invagination; it does not simply throw the cytoskeletal “on” switch. Finally, studies of Drosophila gastrulation have provided insight into how global tissue mechanics and movements are intertwined as multiple tissues simultaneously change shape. Overall, these studies have contributed to the view that cells respond to forces that propagate over great distances, demonstrating that cellular decisions, and, ultimately, tissue shape changes, proceed by integrating cues across an entire embryo.

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Wen, Fu-Lai, Chun Wai Kwan, Yu-Chiun Wang, and Tatsuo Shibata. "Autonomous epithelial folding induced by an intracellular mechano–polarity feedback loop." PLOS Computational Biology 17, no. 12 (December 6, 2021): e1009614. http://dx.doi.org/10.1371/journal.pcbi.1009614.

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Epithelial tissues form folded structures during embryonic development and organogenesis. Whereas substantial efforts have been devoted to identifying mechanical and biochemical mechanisms that induce folding, whether and how their interplay synergistically shapes epithelial folds remains poorly understood. Here we propose a mechano–biochemical model for dorsal fold formation in the early Drosophila embryo, an epithelial folding event induced by shifts of cell polarity. Based on experimentally observed apical domain homeostasis, we couple cell mechanics to polarity and find that mechanical changes following the initial polarity shifts alter cell geometry, which in turn influences the reaction-diffusion of polarity proteins, thus forming a feedback loop between cell mechanics and polarity. This model can induce spontaneous fold formation in silico, recapitulate polarity and shape changes observed in vivo, and confer robustness to tissue shape change against small fluctuations in mechanics and polarity. These findings reveal emergent properties of a developing epithelium under control of intracellular mechano–polarity coupling.

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ONOE, Hiroaki, and Shoji TAKEUCHI. "713 Cell Origami : The Construction of 3D Cellular Tissue by Origami Folding." Proceedings of the Dynamics & Design Conference 2012 (2012): _713–1_—_713–3_. http://dx.doi.org/10.1299/jsmedmc.2012._713-1_.

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WATANABE, Masahiro, Mamoru UEDA, Ryosuke KUBOTA, Rio MIN, Katsuya TANAKA, and Toshihiko TAKENOBU. "A case of folding of the retrodiscal tissue of the temporomandibular joint." Japanese Journal of Oral and Maxillofacial Surgery 69, no. 12 (December 20, 2023): 562–66. http://dx.doi.org/10.5794/jjoms.69.562.

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Denzel, Angela, Maurizio Molinari, Cesar Trigueros, Joanne E. Martin, Shanti Velmurgan, Sue Brown, Gordon Stamp, and Michael J. Owen. "Early Postnatal Death and Motor Disorders in Mice Congenitally Deficient in Calnexin Expression." Molecular and Cellular Biology 22, no. 21 (November 1, 2002): 7398–404. http://dx.doi.org/10.1128/mcb.22.21.7398-7404.2002.

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ABSTRACT Calnexin is a ubiquitously expressed type I membrane protein which is exclusively localized in the endoplasmic reticulum (ER). In mammalian cells, calnexin functions as a chaperone molecule and plays a key role in glycoprotein folding and quality control within the ER by interacting with folding intermediates via their monoglucosylated glycans. In order to gain more insight into the physiological roles of calnexin, we have generated calnexin gene-deficient mice. Despite its profound involvement in protein folding, calnexin is not essential for mammalian-cell viability in vivo: calnexin gene knockout mice were carried to full term, although 50% died within 48 h and the majority of the remaining mice had to be sacrificed within 4 weeks, with only a very few mice surviving to 3 months. Calnexin gene-deficient mice were smaller than their littermates and showed very obvious motor disorders, associated with a dramatic loss of large myelinated nerve fibers. Thus, the critical contribution of calnexin to mammalian physiology is tissue specific.

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Sriharsha, Tirumalasetty, Raghav Raj J., Sudha Venkatesan, Nooka M. Reddy, Vikrannth V., Vinod Raghavan, and Kannan Rajendran. "A rare presentation of amyloid goiter with renal amyloidosis in a young female." International Journal of Advances in Medicine 10, no. 4 (March 24, 2023): 304–6. http://dx.doi.org/10.18203/2349-3933.ijam20230706.

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Amyloidosis is a rare systemic disorder caused by abnormal folding of normal soluble proteins leading to fibril formation in one or more body organs, systems or soft tissues. Amyloid goiter is characterized by deposits of amyloid protein in the thyroid tissue. Amyloid infiltration of thyroid gland with development of secondary goiter is rare. Here we report a case of 36-year-old female presented with progressive painless swelling over neck. Thyroid profile was normal. Ultrasound neck showed enlarged bilateral thyroid gland and isthmus. Fine needle aspiration cytology suggestive of subacute thyroiditis (granulomatous thyroiditis). Total thyroidectomy was done and biopsy sample revealed amyloid goiter.

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Oldmixon, E. H., and F. G. Hoppin. "Alveolar septal folding and lung inflation history." Journal of Applied Physiology 71, no. 6 (December 1, 1991): 2369–79. http://dx.doi.org/10.1152/jappl.1991.71.6.2369.

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On the basis of microscopic appearance of excised lungs, it has been thought that alveolar septa may fold and unfold during deflation and inflation. We suspected that this appearance might depend heavily on the inflation history of the lung preparation. We therefore studied, by light and electron microscopy, dog, rabbit, and rat lungs fixed over a range of inflation pressures and after a variety of inflation histories. Septal folding, as suggested by the configurations of the air spaces, by the placement of the fine and coarse connective tissue elements, and by the pattern of infolding of alveolar epithelium, was readily seen with some inflation protocols but was absent with others. Pressure at fixation was not as important as events before fixation; deflation to 3 cmH2O did not induce folding, and inflation to 16 cmH2O did not undo the folds. This range corresponds with concepts of critical opening and closing pressures. We suggest that folds form de novo during experimental preparation; one need not postulate that septal folding was present in vivo.

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Matus, Soledad, Vicente Valenzuela, Danilo B. Medinas, and Claudio Hetz. "ER Dysfunction and Protein Folding Stress in ALS." International Journal of Cell Biology 2013 (2013): 1–12. http://dx.doi.org/10.1155/2013/674751.

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Amyotrophic lateral sclerosis (ALS) is the most frequent paralytic disease in adults. Most ALS cases are considered sporadic with no clear genetic component. The disruption of protein homeostasis due to chronic stress responses at the endoplasmic reticulum (ER) and the accumulation of abnormal protein inclusions are extensively described in ALS mouse models and patient-derived tissue. Recent studies using pharmacological and genetic manipulation of the unfolded protein response (UPR), an adaptive reaction against ER stress, have demonstrated a complex involvement of the pathway in experimental models of ALS. In addition, quantitative changes in ER stress-responsive chaperones in body fluids have been proposed as possible biomarkers to monitor the disease progression. Here we review most recent advances attributing a causal role of ER stress in ALS.

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Long, Katherine R., and Wieland B. Huttner. "How the extracellular matrix shapes neural development." Open Biology 9, no. 1 (January 2019): 180216. http://dx.doi.org/10.1098/rsob.180216.

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During development, both cells and tissues must acquire the correct shape to allow their proper function. This is especially relevant in the nervous system, where the shape of individual cell processes, such as the axons and dendrites, and the shape of entire tissues, such as the folding of the neocortex, are highly specialized. While many aspects of neural development have been uncovered, there are still several open questions concerning the mechanisms governing cell and tissue shape. In this review, we discuss the role of the extracellular matrix (ECM) in these processes. In particular, we consider how the ECM regulates cell shape, proliferation, differentiation and migration, and more recent work highlighting a key role of ECM in the morphogenesis of neural tissues.

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Terada, Kazutoyo, Masaki Kanazawa, Bernd Bukau, and Masataka Mori. "The Human DnaJ Homologue dj2 Facilitates Mitochondrial Protein Import and Luciferase Refolding." Journal of Cell Biology 139, no. 5 (December 1, 1997): 1089–95. http://dx.doi.org/10.1083/jcb.139.5.1089.

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DnaJ homologues function in cooperation with hsp70 family members in various cellular processes including intracellular protein trafficking and folding. Three human DnaJ homologues present in the cytosol have been identified: dj1 (hsp40/hdj-1), dj2 (HSDJ/hdj-2), and neuronal tissue-specific hsj1. dj1 is thought to be engaged in folding of nascent polypeptides, whereas functions of the other DnaJ homologues remain to be elucidated. To investigate roles of dj2 and dj1, we developed a system of chaperone depletion from and readdition to rabbit reticulocyte lysates. Using this system, we found that heat shock cognate 70 protein (hsc70) and dj2, but not dj1, are involved in mitochondrial import of preornithine transcarbamylase. Bacterial DnaJ could replace mammalian dj2 in mitochondrial protein import. We also tested the effects of these DnaJ homologues on folding of guanidine-denatured firefly luciferase. Unexpectedly, dj2, but not dj1, together with hsc70 refolded the protein efficiently. We propose that dj2 is the functional partner DnaJ homologue of hsc70 in the mammalian cytosol. Bacterial DnaJ protein could replace mammalian dj2 in the refolding of luciferase. Thus, the cytosolic chaperone system for mitochondrial protein import and for protein folding is highly conserved, involving DnaK and DnaJ in bacteria, Ssa1–4p and Ydj1p in yeast, and hsc70 and dj2 in mammals.

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Shirshakova, Maria, Elena Morozova, Daria Sokolova, Svetlana Pervykh, and Lyailya Kayumova. "Cosmetic Syndrome Correction with Calcium Hydroxylapatite-Based Filler in Patients with Connective Tissue Dysplasia." Dermatology Research and Practice 2021 (April 14, 2021): 1–7. http://dx.doi.org/10.1155/2021/6673058.

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Undifferentiated connective tissue dysplasia is one of the most common diseases of nowadays, which does not fit into the group of hereditary syndromes. This condition is diagnosed in 20–50% of the population at any age. The study aimed to correct the facial soft tissues of patients with undifferentiated connective tissue dysplasia through the cosmetic procedure of calcium hydroxylapatite injection. In 2018, a 36-year-old patient addressed the beauty salon with signs of undifferentiated connective tissue dysplasia, such as severe asymmetry of the face, infraorbital and nasolabial sulci, and thin and easily folding skin. Signs were observed from the age of 22, i.e., for 14 years. The therapy was performed using special features of the correction of facial soft tissue changes in patients with connective tissue dysplasia (CTD) using calcium hydroxylapatite-based products (Radiesse®, Merz North America, Inc., USA). Particular attention is given to the need for early correction to prevent premature skin aging related to this condition. After 14 days, a significant improvement of the patient’s skin condition was noted after the passing of two procedures. Her condition was estimated as consistent with T1-2P0G0A1Zh1 P1M1K1 and corresponded to grade I age-related changes in the superficial soft tissues. The performed treatment showed high efficacy in case of mild connective tissue dysplasia diagnosis. The results showed that when collecting information from anamnesis, the diagnostic criteria for dysplasia should be considered. If the criteria are met, the cosmetological correction with collagen stimulators becomes possible.

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Eritano, Anthony S., Claire L. Bromley, Antonio Bolea Albero, Lucas Schütz, Fu-Lai Wen, Michiko Takeda, Takashi Fukaya, et al. "Tissue-Scale Mechanical Coupling Reduces Morphogenetic Noise to Ensure Precision during Epithelial Folding." Developmental Cell 53, no. 2 (April 2020): 212–28. http://dx.doi.org/10.1016/j.devcel.2020.02.012.

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Ionov, Leonid, Svetlana Zakharchenko, and Georgi Stoychev. "Soft Microorigami: Stimuli-Responsive Self-Folding Polymer Films." Advances in Science and Technology 77 (September 2012): 348–53. http://dx.doi.org/10.4028/www.scientific.net/ast.77.348.

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Asymmetry is intrinsic to natural systems and is widely used by living organisms for efficient adaptation, mimicry and movement. Polymer bilayers are the example of synthetic asymmetric systems, which are able to generate macroscopic motion and fold by forming different 3D objects such as tubes and capsules. Similar to bimetal films, the polymer bilayer consist of two substances with different swelling properties. One polymer is non-swellable and hydrophobic. Another polymer is water-swellable hydrogel. The folding, which might occur in response to temperature or pH, is caused by swelling of the hydrogel layer. The formed tubes and capsules can be manipulated using magnetic field. Reversible folding and unfolding of the polymer films is applied for reversible capture and release of cells in response to change of temperature and other signals. This novel biomimetic approach can be used for controlled encapsulation and release of microparticles, cells and drugs as well as fabrication of 3D scaffolds for tissue engineering.

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Meng, Xiang-Sen, Li-Chuan Zhou, Lei Liu, Yin-Bo Zhu, Yu-Feng Meng, Dong-Chang Zheng, Bo Yang, et al. "Deformable hard tissue with high fatigue resistance in the hinge of bivalve Cristaria plicata." Science 380, no. 6651 (June 23, 2023): 1252–57. http://dx.doi.org/10.1126/science.ade2038.

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The hinge of bivalve shells can sustain hundreds of thousands of repeating opening-and-closing valve motions throughout their lifetime. We studied the hierarchical design of the mineralized tissue in the hinge of the bivalve Cristaria plicata , which endows the tissue with deformability and fatigue resistance and consequently underlies the repeating motion capability. This folding fan–shaped tissue consists of radially aligned, brittle aragonite nanowires embedded in a resilient matrix and can translate external radial loads to circumferential deformation. The hard-soft complex microstructure can suppress stress concentration within the tissue. Coherent nanotwin boundaries along the longitudinal direction of the nanowires increase their resistance to bending fracture. The unusual biomineral, which exploits the inherent properties of each component through multiscale structural design, provides insights into the evolution of antifatigue structural materials.

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Karbaschi, Mohammad Reza, Brett Williams, Acram Taji, and Sagadevan G. Mundree. "Tripogon loliiformis elicits a rapid physiological and structural response to dehydration for desiccation tolerance." Functional Plant Biology 43, no. 7 (2016): 643. http://dx.doi.org/10.1071/fp15213.

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Resurrection plants can withstand extreme dehydration to an air-dry state and then recover upon receiving water. Tripogon loliiformis (F.Muell.) C.E.Hubb. is a largely uncharacterised native Australian desiccation-tolerant grass that resurrects from the desiccated state within 72 h. Using a combination of structural and physiological techniques the structural and physiological features that enable T. loliiformis to tolerate desiccation were investigated. These features include: (i) a myriad of structural changes such as leaf folding, cell wall folding and vacuole fragmentation that mitigate desiccation stress, (ii) potential role of sclerenchymatous tissue within leaf folding and radiation protection, (iii) retention of ~70% chlorophyll in the desiccated state, (iv) early response of photosynthesis to dehydration by 50% reduction and ceasing completely at 80 and 70% relative water content, respectively, (v) a sharp increase in electrolyte leakage during dehydration, and (vi) confirmation of membrane integrity throughout desiccation and rehydration. Taken together, these results demonstrate that T. loliiformis implements a range of structural and physiological mechanisms that minimise mechanical, oxidative and irradiation stress. These results provide powerful insights into tolerance mechanisms for potential utilisation in the enhancement of stress-tolerance in crop plants.

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Kim, P. S., O. Y. Kwon, and P. Arvan. "An endoplasmic reticulum storage disease causing congenital goiter with hypothyroidism." Journal of Cell Biology 133, no. 3 (May 1, 1996): 517–27. http://dx.doi.org/10.1083/jcb.133.3.517.

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In humans, deficient thyroglobulin (Tg, the thyroid prohormone) is an important cause of congenital hypothyroid goiter; further, homozygous mice expressing two cog/cog alleles (linked to the Tg locus) exhibit the same phenotype. Tg mutations might affect multiple different steps in thyroid hormone synthesis; however, the microscopic and biochemical phenotype tends to involve enlargement of the thyroid ER and accumulation of protein bands of M(r) < 100. To explore further the cell biology of this autosomal recessive illness, we have examined the folding and intracellular transport of newly synthesized Tg in cog/cog thyroid tissue. We find that mutant mice synthesize a full-length Tg, which appears to undergo normal N-linked glycosylation and glucose trimming. Nevertheless, in the mutant, Tg is deficient in the folding that leads to homodimerization, and there is a deficiency in the quantity of intracellular Tg transported to the distal portion of the secretory pathway. Indeed, we find that the underlying disorder in cog/cog mice is a thyroid ER storage disease, in which a temperature-sensitive Tg folding defect, in conjunction with normal ER quality control mechanisms, leads to defective Tg export. In relation to quality control, we find that the physiological response in this illness includes the specific induction of five molecular chaperones in the thyroid ER. Based on the pattern of chaperone binding, different potential roles for individual chaperones are suggested in glycoprotein folding, retention, and degradation in this ER storage disease.

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Liu, Zihan, Jorge Alemán-Báez, Richard G. F. Visser, and Guusje Bonnema. "Cabbage (Brassica oleracea var. capitata) Development in Time: How Differential Parenchyma Tissue Growth Affects Leafy Head Formation." Plants 13, no. 5 (February 27, 2024): 656. http://dx.doi.org/10.3390/plants13050656.

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This study aims to categorize the morphological changes during cabbage (B. oleracea ssp. capitata) development, seedling, rosette, folding, and heading, and to elucidate the cellular mechanisms of the leaf curvature, essential for the formation of the leafy head. We followed the growth of two cabbage cultivars with distinct head shapes (round and pointed) and one non-heading collard cultivar; we phenotyped the size and volume of the whole plant as well as the size, shape, and curvature of the leaves during growth. By integrating these phenotypic data, we determined the four vegetative stages for both cabbages. The histological phenotypes of microtome sections from five distinct leaf positions of the rosette, folding, and heading leaves at two timepoints during leaf growth were quantified and revealed variations in cellular parameters among leaf types, between leaf positions, and between the adaxial and abaxial sides. We identified two synergistic cellular mechanisms contributing to the curvature of heading leaves: differential growth across the leaf blade, with increased growth at the leaf’s center relative to the margins; and the increased expansion of the spongy parenchyma layer compared to the palisade parenchyma layer, resulting in the direction of the curvature, which is inwards. These two processes together contribute to the typical leafy heads of cabbages.

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Fal, Kateryna, Niklas Korsbo, Juan Alonso-Serra, Jose Teles, Mengying Liu, Yassin Refahi, Marie-Edith Chabouté, Henrik Jönsson, and Olivier Hamant. "Tissue folding at the organ–meristem boundary results in nuclear compression and chromatin compaction." Proceedings of the National Academy of Sciences 118, no. 8 (February 19, 2021): e2017859118. http://dx.doi.org/10.1073/pnas.2017859118.

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Artificial mechanical perturbations affect chromatin in animal cells in culture. Whether this is also relevant to growing tissues in living organisms remains debated. In plants, aerial organ emergence occurs through localized outgrowth at the periphery of the shoot apical meristem, which also contains a stem cell niche. Interestingly, organ outgrowth has been proposed to generate compression in the saddle-shaped organ–meristem boundary domain. Yet whether such growth-induced mechanical stress affects chromatin in plant tissues is unknown. Here, by imaging the nuclear envelope in vivo over time and quantifying nucleus deformation, we demonstrate the presence of active nuclear compression in that domain. We developed a quantitative pipeline amenable to identifying a subset of very deformed nuclei deep in the boundary and in which nuclei become gradually narrower and more elongated as the cell contracts transversely. In this domain, we find that the number of chromocenters is reduced, as shown by chromatin staining and labeling, and that the expression of linker histone H1.3 is induced. As further evidence of the role of forces on chromatin changes, artificial compression with a MicroVice could induce the ectopic expression of H1.3 in the rest of the meristem. Furthermore, while the methylation status of chromatin was correlated with nucleus deformation at the meristem boundary, such correlation was lost in the h1.3 mutant. Altogether, we reveal that organogenesis in plants generates compression that is able to have global effects on chromatin in individual cells.

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Naglieri, Valentina. "Bio Focus: Nanopatterned self-folding origami may open up new possibilities in tissue engineering." MRS Bulletin 41, no. 11 (November 2016): 840. http://dx.doi.org/10.1557/mrs.2016.253.

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Wiréhn, Jimmy, Karin Carlsson, Anna Herland, Egon Persson, Uno Carlsson, Magdalena Svensson, and Per Hammarström. "Activity, Folding, Misfolding, and Aggregationin Vitroof the Naturally Occurring Human Tissue Factor Mutant R200W†." Biochemistry 44, no. 18 (May 2005): 6755–63. http://dx.doi.org/10.1021/bi047388l.

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Vasiev, Iskandar, Andrew I. M. Greer, Ali Z. Khokhar, John Stormonth-Darling, K. Elizabeth Tanner, and Nikolaj Gadegaard. "Self-folding nano- and micropatterned hydrogel tissue engineering scaffolds by single step photolithographic process." Microelectronic Engineering 108 (August 2013): 76–81. http://dx.doi.org/10.1016/j.mee.2013.04.003.

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Journal articles on the topic 'Tissue folding'

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