Single cell transplantation reveals interspecific cell communication in Drosophila chimeras

Development ◽  
1990 ◽  
Vol 109 (4) ◽  
pp. 821-832 ◽  
Author(s):  
T. Becker ◽  
G.M. Technau

Cell-cell communication is not only a common strategy for cell fate specification in vertebrates, but plays important roles in invertebrate development as well. We report here on experiments testing the compatibility of mechanisms specifying cell fate among six different Drosophila species. Following interspecific transplantation, the development of single ectodermal cells was traced in order to test their abilities to proliferate and differentiate in a heterologous environment. Despite considerable differences in cell size and length of cell cycle among some of the species, the transplants gave rise to fully differentiated clones that were integrated into the host tissue. Clones comprised cells of epidermal and/or neural histotypes, indicating that mechanisms mediating the epidermal/neural dichotomy in the ectoderm are conserved between the species. Cells of the neural lineages differentiated into neurones, glia, or both. Moreover, heterologous neurones sent out axons that followed major pathways along nerves and within the neuropile, demonstrating their ability to recognize positional cues in the heterologous CNS of the host.

2018 ◽  
Author(s):  
Chaitanya Dingare ◽  
Alina Niedzwetzki ◽  
Petra A Klemmt ◽  
Svenja Godbersen ◽  
Ricardo Fuentes ◽  
...  

SUMMARYIn the last decade, Hippo signaling has emerged as a critical pathway integrating extrinsic and intrinsic mechanical cues to regulate cell proliferation and survival, tissue morphology and organ size in vivo. Despite its essential role in organogenesis, surprisingly much less is known about how it connects biomechanical signals to control of cell fate and cell size during development. Here we unravel a novel and unexpected role of the Hippo pathway effector Taz (wwtr1) in the control of cell size and cell fate specification. In teleosts, fertilization occurs through a specific structure at the animal pole, called the micropyle. This opening in the chorion is formed during oogenesis by a specialized somatic follicle cell, the micropylar cell (MC). The MC has a peculiar shape and is much larger than its neighboring follicle cells but the mechanisms underlying its specification and cell shape acquisition are not known. Here we show that Taz is essential for the specification of the MC and subsequent micropyle formation in zebrafish. We identify Taz as the first bona fide MC marker and show that Taz is specifically and strongly enriched in the MC precursor before the cell can be identified morphologically. Altogether, our genetic data and molecular characterization of the MC lead us to propose that Taz is a key regulator of the MC fate activated by physical cues emanating from the oocyte to initiate the MC morphogenetic program. We describe here for the first time the mechanism underlying the specification of the MC fate.


2021 ◽  
Vol 12 ◽  
Author(s):  
Laura Serrano-Ron ◽  
Javier Cabrera ◽  
Pablo Perez-Garcia ◽  
Miguel A. Moreno-Risueno

Over the last decades, research on postembryonic root development has been facilitated by “omics” technologies. Among these technologies, microarrays first, and RNA sequencing (RNA-seq) later, have provided transcriptional information on the underlying molecular processes establishing the basis of System Biology studies in roots. Cell fate specification and development have been widely studied in the primary root, which involved the identification of many cell type transcriptomes and the reconstruction of gene regulatory networks (GRN). The study of lateral root (LR) development has not been an exception. However, the molecular mechanisms regulating cell fate specification during LR formation remain largely unexplored. Recently, single-cell RNA-seq (scRNA-seq) studies have addressed the specification of tissues from stem cells in the primary root. scRNA-seq studies are anticipated to be a useful approach to decipher cell fate specification and patterning during LR formation. In this review, we address the different scRNA-seq strategies used both in plants and animals and how we could take advantage of scRNA-seq to unravel new regulatory mechanisms and reconstruct GRN. In addition, we discuss how to integrate scRNA-seq results with previous RNA-seq datasets and GRN. We also address relevant findings obtained through single-cell based studies and how LR developmental studies could be facilitated by scRNA-seq approaches and subsequent GRN inference. The use of single-cell approaches to investigate LR formation could help to decipher fundamental biological mechanisms such as cell memory, synchronization, polarization, or pluripotency.


Development ◽  
2019 ◽  
Vol 146 (17) ◽  
pp. dev178103 ◽  
Author(s):  
Quentin Lo Giudice ◽  
Marion Leleu ◽  
Gioele La Manno ◽  
Pierre J. Fabre

Development ◽  
1995 ◽  
Vol 121 (11) ◽  
pp. 3713-3721 ◽  
Author(s):  
K. Weigmann ◽  
C.F. Lehner

The correct specification of defined neurons in the Drosophila central nervous system is dependent on even-skipped. During CNS development, even-skipped expression starts in the ganglion mother cell resulting from the first asymmetric division of neuroblast NB 1–1. This first division of NB 1–1 (and of the other early neuroblasts as well) is temporally controlled by the transcriptional regulation of string expression, which we have manipulated experimentally, even-skipped expression still occurs if the first neuroblast division is delayed, but not if the division is prohibited. Moreover, even-skipped expression is also dependent on progression through S phase which follows immediately after the first division. However, cytokinesis during the first NB division is not required for even-skipped expression as revealed by observations in pebble mutant embryos. Our results demonstrate therefore that even-skipped expression is coupled to cell cycle progression, presumably in order to prevent a premature activation of expression by a positive regulator which is produced already in the neuroblast during G2 and segregated asymmetrically into the ganglion mother cell during mitosis.


2020 ◽  
Vol 98 (1) ◽  
pp. 50-60 ◽  
Author(s):  
Connor O’Sullivan ◽  
Philip E.B. Nickerson ◽  
Oliver Krupke ◽  
Jennifer Christie ◽  
Li-Li Chen ◽  
...  

During a developmental period that extends postnatally in the mouse, proliferating multipotent retinal progenitor cells produce one of 7 major cell types (rod, cone, bipolar, horizontal, amacrine, ganglion, and Müller glial cells) as they exit the cell cycle in consecutive waves. Cell production in the retina is tightly regulated by intrinsic, extrinsic, spatial, and temporal cues, and is coupled to the timing of cell cycle exit. Arsenic-resistance protein 2 (ARS2, also known as SRRT) is a component of the nuclear cap-binding complex involved in RNA Polymerase II transcription, and is required for cell cycle progression. We show that postnatal retinal progenitor cells (RPCs) require ARS2 for proper progression through S phase, and ARS2 disruption leads to early exit from the cell cycle. Furthermore, we observe an increase in the proportion of cells expressing a rod photoreceptor marker, and a loss of Müller glia marker expression, indicating a role for ARS2 in regulating cell fate specification or differentiation. Knockdown of Flice Associated Huge protein (FLASH), which interacts with ARS2 and is required for cell cycle progression and 3′-end processing of replication-dependent histone transcripts, phenocopies ARS2 knockdown. These data implicate ARS2–FLASH-mediated histone mRNA processing in regulating RPC cell cycle kinetics and neuroglial cell fate specification during postnatal retinal development.


2018 ◽  
Vol 29 (3) ◽  
pp. 1280-1290 ◽  
Author(s):  
Gewei Lian ◽  
Timothy Wong ◽  
Jie Lu ◽  
Jianjun Hu ◽  
Jingping Zhang ◽  
...  

Abstract Neural progenitor proliferation and cell fate decision from self-renewal to differentiation are crucial factors in determining brain size and morphology. The cytoskeletal dependent regulation of these processes is not entirely known. The actin-binding filamin A (FlnA) was shown to regulate proliferation of progenitors by directing changes in cell cycles proteins such as Cdk1 during G2/M phase. Here we report that functional loss of FlnA not only affects the rate of proliferation by altering cell cycle length but also causes a defect in early differentiation through changes in cell fate specification. FlnA interacts with Rho GTPase RhoA, and FlnA loss impairs RhoA activation. Disruption of either of these cytoskeletal associated proteins delays neurogenesis and promotes neural progenitors to remain in proliferative states. Aurora kinase B (Aurkb) has been implicated in cytokinesis, and peaks in expression during the G2/M phase. Inhibition of FlnA or RhoA impairs Aurkb degradation and alters its localization during mitosis. Overexpression of Aurkb replicates the same delay in neurogenesis seen with loss of FlnA or RhoA. Our findings suggest that shared cytoskeletal processes can direct neural progenitor proliferation by regulating the expression and localization of proteins that are implicated in the cell cycle progression and cell fate specification.


2010 ◽  
Vol 337 (2) ◽  
pp. 415-424 ◽  
Author(s):  
Christian Berger ◽  
Ramakrishnan Kannan ◽  
Sudharani Myneni ◽  
Simone Renner ◽  
L.S. Shashidhara ◽  
...  

Nature ◽  
2021 ◽  
Vol 598 (7879) ◽  
pp. 205-213
Author(s):  
Ryan S. Ziffra ◽  
Chang N. Kim ◽  
Jayden M. Ross ◽  
Amy Wilfert ◽  
Tychele N. Turner ◽  
...  

AbstractDuring mammalian development, differences in chromatin state coincide with cellular differentiation and reflect changes in the gene regulatory landscape1. In the developing brain, cell fate specification and topographic identity are important for defining cell identity2 and confer selective vulnerabilities to neurodevelopmental disorders3. Here, to identify cell-type-specific chromatin accessibility patterns in the developing human brain, we used a single-cell assay for transposase accessibility by sequencing (scATAC-seq) in primary tissue samples from the human forebrain. We applied unbiased analyses to identify genomic loci that undergo extensive cell-type- and brain-region-specific changes in accessibility during neurogenesis, and an integrative analysis to predict cell-type-specific candidate regulatory elements. We found that cerebral organoids recapitulate most putative cell-type-specific enhancer accessibility patterns but lack many cell-type-specific open chromatin regions that are found in vivo. Systematic comparison of chromatin accessibility across brain regions revealed unexpected diversity among neural progenitor cells in the cerebral cortex and implicated retinoic acid signalling in the specification of neuronal lineage identity in the prefrontal cortex. Together, our results reveal the important contribution of chromatin state to the emerging patterns of cell type diversity and cell fate specification and provide a blueprint for evaluating the fidelity and robustness of cerebral organoids as a model for cortical development.


Sign in / Sign up

Export Citation Format

Share Document