scholarly journals Duplication of Spiralian-Specific TALE Genes And Evolution of The Blastomere Specification Mechanism In The Bivalve Lineage

2021 ◽  
Author(s):  
Supanat Phuangphong ◽  
Jumpei Tsunoda ◽  
Hiroshi Wada ◽  
Yoshiaki Morino
Keyword(s):  
Cell Fate ◽  
Early Development ◽  
Functional Divergence ◽  
Expression Patterns ◽  
Fate Map ◽  
Cell Fates ◽  
Cell Specification ◽  
Cytoplasmic Content ◽  
Gene Regulatory ◽  
Unique Cell

Abstract Background Despite the conserved pattern of the cell-fate map among spiralians, bivalves display several modified characteristics during their early development, including early specification of the D blastomere by the cytoplasmic content, as well as the distinctive fate of the 2d blastomere. However, it is unclear what changes in gene regulatory mechanisms led to such changes in cell specification patterns. Spiralian-TALE (SPILE) genes are a group of spiralian-specific transcription factors that play a role in specifying blastomere cell fates during early development in limpets. We hypothesised that the expansion of SPILE gene repertoires influenced the evolution of the specification pattern of blastomere cell fates.Results We performed a transcriptome analysis of early development in the purplish bifurcate mussel and identified 13 SPILE genes. Phylogenetic analysis of the SPILE gene in bivalves and limpets suggested that extra duplications of SPILE genes occurred in the bivalve lineage. We examined the expression patterns of the SPILE gene in mussels and found that some SPILE genes were expressed in quartet-specific patterns, as observed in limpets. Furthermore, we found that several SPILE genes that had undergone gene duplication were specifically expressed in the D quadrant, C and D quadrants or the 2d blastomere. These expression patterns were distinct from the expression patterns of SPILE in their limpet counterparts. Conclusions These results suggest that, in addition to their ancestral role in quartet specification, bivalve SPILE genes contributed to the specification of C and D quadrants. We propose that the expansion of SPILE genes in the bivalve lineage created extra SPILE genes that underwent expression pattern and functional divergence, thereby resulting in the evolution of a unique cell-fate specification pattern in bivalves.

scholarly journals Duplication of spiralian-specific TALE genes and evolution of the blastomere specification mechanism in the bivalve lineage

EvoDevo ◽  
2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Supanat Phuangphong ◽  
Jumpei Tsunoda ◽  
Hiroshi Wada ◽  
Yoshiaki Morino
Keyword(s):  
Cell Fate ◽  
Early Development ◽  
Expression Patterns ◽  
Cell Fate Specification ◽  
Fate Map ◽  
Cell Fates ◽  
Cell Specification ◽  
Cytoplasmic Content ◽  
Gene Regulatory ◽  
Unique Cell

Abstract Background Despite the conserved pattern of the cell-fate map among spiralians, bivalves display several modified characteristics during their early development, including early specification of the D blastomere by the cytoplasmic content, as well as the distinctive fate of the 2d blastomere. However, it is unclear what changes in gene regulatory mechanisms led to such changes in cell specification patterns. Spiralian-TALE (SPILE) genes are a group of spiralian-specific transcription factors that play a role in specifying blastomere cell fates during early development in limpets. We hypothesised that the expansion of SPILE gene repertoires influenced the evolution of the specification pattern of blastomere cell fates. Results We performed a transcriptome analysis of early development in the purplish bifurcate mussel and identified 13 SPILE genes. Phylogenetic analysis of the SPILE gene in molluscs suggested that duplications of SPILE genes occurred in the bivalve lineage. We examined the expression patterns of the SPILE gene in mussels and found that some SPILE genes were expressed in quartet-specific patterns, as observed in limpets. Furthermore, we found that several SPILE genes that had undergone gene duplication were specifically expressed in the D quadrant, C and D quadrants or the 2d blastomere. These expression patterns were distinct from the expression patterns of SPILE in their limpet counterparts. Conclusions These results suggest that, in addition to their ancestral role in quartet specification, certain SPILE genes in mussels contribute to the specification of the C and D quadrants. We suggest that the expansion of SPILE genes in the bivalve lineage contributed to the evolution of a unique cell fate specification pattern in bivalves.

scholarly journals A gene expression atlas of abicoid-depleted Drosophila embryo reveals early canalization of cell fate

2014 ◽  
Author(s):  
Max V Staller ◽  
Charless C Fowlkes ◽  
Meghan D.J. Bragdon ◽  
Zeba B. Wunderlich ◽  
Angela DePace
Keyword(s):  
Gene Expression ◽  
Cell Fate ◽  
Early Stage ◽  
Expression Patterns ◽  
Drosophila Embryo ◽  
Wild Type ◽  
Cell Fates ◽  
Gene Expression Atlas ◽  
Expression Atlas ◽  
Gene Regulatory

In developing embryos, gene regulatory networks canalize cells towards discrete terminal fates. We studied the behavior of the anterior-posterior segmentation network in Drosophila melanogaster embryos depleted of a key maternal input, bicoid (bcd), by building a cellular- resolution gene expression atlas containing measurements of 12 core patterning genes over 6 time points in early development. With this atlas, we determine the precise perturbation each cell experiences, relative to wild type, and observe how these cells assume cell fates in the perturbed embryo. The first zygotic layer of the network, consisting of the gap and terminal genes, is highly robust to perturbation: all combinations of transcription factor expression found in bcd depleted embryos were also found in wild type embryos, suggesting that no new cell fates were created even at this very early stage. All of the gap gene expression patterns in the trunk expand by different amounts, a feature that we were unable to explain using two simple models of the effect of bcd depletion. In the second layer of the network, depletion of bcd led to an excess of cells expressing both even skipped and fushi tarazu early in the blastoderm stage, but by gastrulation this overlap resolved into mutually exclusive stripes. Thus, following depletion of bcd, individual cells rapidly canalize towards normal cell fates in both layers of this gene regulatory network. Our gene expression atlas provides a high resolution picture of a classic perturbation and will enable further modeling of canalization in this transcriptional network.

scholarly journals Joint profiling of gene expression and chromatin accessibility of amphioxus development at single cell resolution

2021 ◽  
Author(s):  
Pengcheng Ma ◽  
Xingyan Liu ◽  
Huimin Liu ◽  
Zaoxu Xu ◽  
Xiangning Ding ◽  
...  
Keyword(s):  
Gene Expression ◽  
Single Cell ◽  
Cell Fate ◽  
Regulatory Networks ◽  
Functional Divergence ◽  
Expression Patterns ◽  
Genetic Regulatory Networks ◽  
Public Access ◽  
Origin And Evolution ◽  
Key Species

Abstract Vertebrate evolution was accompanied with two rounds of whole genome duplication followed by functional divergence in terms of regulatory circuits and gene expression patterns. As a basal and slow-evolving chordate species, amphioxus is an ideal paradigm for exploring the origin and evolution of vertebrates. Single cell sequencing has been widely employed to construct the developmental cell atlas of several key species of vertebrates (human, mouse, zebrafish and frog) and tunicate (sea squirts). Here, we performed single-nucleus RNA sequencing (snRNA-seq) and single-cell assay for transposase accessible chromatin sequencing (scATAC-seq) for different stages of amphioxus (covering embryogenesis and adult tissues). With the datasets generated we constructed the developmental tree for amphioxus cell fate commitment and lineage specification, and revealed the underlying key regulators and genetic regulatory networks. The generated data were integrated into an online platform, AmphioxusAtlas, for public access at http://120.79.46.200:81/AmphioxusAtlas.

Feedback regulation is central to Delta-Notch signalling required for Drosophila wing vein morphogenesis

Development ◽  
1997 ◽  
Vol 124 (17) ◽  
pp. 3283-3291 ◽  
Author(s):  
S.S. Huppert ◽  
T.L. Jacobsen ◽  
M.A. Muskavitch
Keyword(s):  
Protein Expression ◽  
Cell Fate ◽  
Expression Patterns ◽  
Feedback Regulation ◽  
Notch Signalling ◽  
Notch Receptor ◽  
Cell Fates ◽  
Wing Vein ◽  
Drosophila Wing ◽  
Puparium Formation

Delta and Notch are required for partitioning of vein and intervein cell fates within the provein during Drosophila metamorphosis. We find that partitioning of these fates is dependent on Delta-mediated signalling from 22 to 30 hours after puparium formation at 25 degrees C. Within the provein, Delta is expressed more highly in central provein cells (presumptive vein cells) and Notch is expressed more highly in lateral provein cells (presumptive intervein cells). Accumulation of Notch in presumptive intervein cells is dependent on Delta signalling activity in presumptive vein cells and constitutive Notch receptor activity represses Delta accumulation in presumptive vein cells. When Delta protein expression is elevated ectopically in presumptive intervein cells, complementary Delta and Notch expression patterns in provein cells are reversed, and vein loss occurs because central provein cells are unable to stably adopt the vein cell fate. Our findings imply that Delta-Notch signalling exerts feedback regulation on Delta and Notch expression during metamorphic wing vein development, and that the resultant asymmetries in Delta and Notch expression underlie the proper specification of vein and intervein cell fates within the provein.

Cell movements and cell fate during zebrafish gastrulation

Development ◽  
1992 ◽  
Vol 116 (Supplement) ◽  
pp. 65-73 ◽  
Author(s):  
Robert K. Ho
Keyword(s):  
Single Cell ◽  
Cell Fate ◽  
Fate Map ◽  
Cell Fates ◽  
Cell Lineages ◽  
Cell Position ◽  
Vertebrate Embryo ◽  
Cellular Identity ◽  
Transplantation Experiments

The early lineages of the zebrafish are indeterminate and a single cell labeled before the late blastula period will contribute progeny to a variety of tissues. Therefore, early cell lineages in the zebrafish do not establish future cell fates and early blastomeres must necessarily remain pluripotent. Eventually, after a period of random cell mixing, individual cells do become tissue restricted according to their later position within the blastoderm. The elucidation of a fate map for the zebrafish gastrula (Kimmel et al., 1990), has made it possible to study the processes by which cellular identity is conferred and maintained in the zebrafish. In this chapter, I describe single cell transplantation experiments designed to test for the irreversible restriction or ‘commitment’ of embryonic blastomeres in the zebrafish embryo. These experiments support the hypothesis that cell fate in the vertebrate embryo is determined by cell position. Work on the spadetail mutation will also be reviewed; this mutation causes a subset of mesodermal precursors to mismigrate during gastrulation thereby leading to a change in their eventual cell identity.

scholarly journals Interdependent regulation of stereotyped and stochastic photoreceptor fates in the fly eye

2019 ◽  
Author(s):  
Adam C. Miller ◽  
Elizabeth Urban ◽  
Eric L. Lyons ◽  
Tory G. Herman ◽  
Robert J. Johnston
Keyword(s):  
Transcription Factor ◽  
Cell Fate ◽  
Gene Networks ◽  
Control Cell ◽  
Regulatory Mechanisms ◽  
Cell Fates ◽  
Feedback Mechanisms ◽  
Fate Specification ◽  
Gene Regulatory ◽  
Fly Eye

AbstractDiversification of neuronal subtypes often requires stochastic gene regulatory mechanisms. How stochastically expressed transcription factors interact with other regulators in gene networks to specify cell fates is poorly understood. The random mosaic of color-detecting R7 photoreceptor subtypes in Drosophila is controlled by the stochastic on/off expression of the transcription factor Spineless (Ss). In SsON R7s, Ss induces expression of Rhodopsin 4 (Rh4), whereas in SsOFF R7s, the absence of Ss allows expression of Rhodopsin 3 (Rh3). Here, we find that the transcription factor Runt, which is initially expressed in all R7s, activates expression of Spineless in a random subset of R7s. Later, as R7s develop, Ss negatively feeds back onto Runt to prevent repression of Rh4 and ensure proper fate specification. Together, stereotyped and stochastic regulatory inputs are integrated into feedforward and feedback mechanisms to control cell fate.

scholarly journals A developmental gene regulatory network for invasive differentiation of theC. elegansanchor cell

2019 ◽  
Author(s):  
Taylor N. Medwig-Kinney ◽  
Jayson J. Smith ◽  
Nicholas J. Palmisano ◽  
Sujata Tank ◽  
Wan Zhang ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Gene Regulatory Network ◽  
Cell Fate ◽  
Regulatory Network ◽  
Cell Biology ◽  
Type I ◽  
Cell Specification ◽  
C Elegans ◽  
Gene Regulatory ◽  
Anchor Cell

ABSTRACTCellular invasion is a key part of development, immunity, and disease. Using thein vivomodel ofC. elegansanchor cell invasion, we characterize the gene regulatory network that promotes invasive differentiation. The anchor cell is initially specified in a stochastic cell fate decision mediated by Notch signaling. Previous research has identified four conserved transcription factors,fos-1a(Fos),egl-43(EVI1/MEL),hlh-2(E/Daughterless) andnhr-67(NR2E1/TLX), that mediate anchor cell specification and/or invasive differentiation. Connections between these transcription factors and the underlying cell biology that they regulate is poorly understood. Here, using genome editing and RNA interference, we examine transcription factor interactions prior to and after anchor cell specification. During invasion we identify thategl-43,hlh-2, andnhr-67function together in a type I coherent feed-forward loop with positive feedback. Conversely, prior to specification, these transcription factors function independent of one another to regulate LIN-12 (Notch) activity. Together, these results demonstrate that, although the same transcription factors can function in fate specification and differentiated cell behavior, a gene regulatory network can be rapidly re-wired to reinforce a post-mitotic, pro-invasive state.SUMMARY STATEMENTBasement membrane invasion by theC. elegansanchor cell is coordinated by a dynamic gene regulatory network encompassing cell cycle dependent and independent sub-circuits.

scholarly journals Bcl11b and combinatorial resolution of cell fate in the T-cell gene regulatory network

2017 ◽  
Vol 114 (23) ◽  
pp. 5800-5807 ◽  
Author(s):  
William J. R. Longabaugh ◽  
Weihua Zeng ◽  
Jingli A. Zhang ◽  
Hiroyuki Hosokawa ◽  
Camden S. Jansen ◽  
...  
Keyword(s):  
Transcription Factors ◽  
T Cell ◽  
Notch Signaling ◽  
Gene Regulatory Network ◽  
Cell Fate ◽  
Regulatory Network ◽  
T Cell Development ◽  
Cell Specification ◽  
Gene Regulatory

T-cell development from hematopoietic progenitors depends on multiple transcription factors, mobilized and modulated by intrathymic Notch signaling. Key aspects of T-cell specification network architecture have been illuminated through recent reports defining roles of transcription factors PU.1, GATA-3, and E2A, their interactions with Notch signaling, and roles of Runx1, TCF-1, and Hes1, providing bases for a comprehensively updated model of the T-cell specification gene regulatory network presented herein. However, the role of lineage commitment factor Bcl11b has been unclear. We use self-organizing maps on 63 RNA-seq datasets from normal and perturbed T-cell development to identify functional targets of Bcl11b during commitment and relate them to other regulomes. We show that both activation and repression target genes can be bound by Bcl11b in vivo, and that Bcl11b effects overlap with E2A-dependent effects. The newly clarified role of Bcl11b distinguishes discrete components of commitment, resolving how innate lymphoid, myeloid, and dendritic, and B-cell fate alternatives are excluded by different mechanisms.

scholarly journals Precision of Tissue Patterning is Controlled by Dynamical Properties of Gene Regulatory Networks

2019 ◽  
Author(s):  
Katherine Exelby ◽  
Edgar Herrera-Delgado ◽  
Lorena Garcia Perez ◽  
Ruben Perez-Carrasco ◽  
Andreas Sagner ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Regulatory Networks ◽  
Regulatory Network ◽  
Regulatory Networks ◽  
Expression Patterns ◽  
Cell Fates ◽  
Gene Circuits ◽  
Stochastic Fluctuations ◽  
Network Properties ◽  
Gene Regulatory

AbstractDuring development, gene regulatory networks allocate cell fates by partitioning tissues into spatially organised domains of gene expression. How the sharp boundaries that delineate these gene expression patterns arise, despite the stochasticity associated with gene regulation, is poorly understood. We show, in the vertebrate neural tube, using perturbations of coding and regulatory regions, that the structure of the regulatory network contributes to boundary precision. This is achieved, not by reducing noise in individual genes, but by the configuration of the network modulating the ability of stochastic fluctuations to initiate gene expression changes. We use a computational screen to identify network properties that influence boundary precision, revealing two dynamical mechanisms by which small gene circuits attenuate the effect of noise in order to increase patterning precision. These results highlight design principles of gene regulatory networks that produce precise patterns of gene expression.

scholarly journals Calpain DEK1 acts as a developmental switch gatekeeping cell fate transitions

2021 ◽  
Author(s):  
Viktor Demko ◽  
Tatiana Belova ◽  
Maxim Messerer ◽  
Torgeir R. Hvidsten ◽  
Pierre-François Perroud ◽  
...  
Keyword(s):  
Cell Fate ◽  
Regulatory Networks ◽  
Data Science ◽  
Control Cell ◽  
Cysteine Proteases ◽  
Regulatory Role ◽  
Phenotypic Traits ◽  
Cell Fates ◽  
Gene Regulatory ◽  
Developmental Switch

SummaryCalpains are cysteine proteases that control cell fate transitions. Although calpains are viewed as modulatory proteases displaying severe, pleiotropic phenotypes in eukaryotes, human calpain targets are also directed to the N-end rule degradatory pathway. Several of these destabilized targets are transcription factors, hinting at a gene regulatory role. Here, we analyze the gene regulatory networks of Physcomitrium patens and characterize the regulons that are deregulated in DEK1 calpain mutants. Predicted cleavage patterns of regulatory hierarchies in the five DEK1-controlled subnetworks are consistent with the gene’s pleiotropy and the regulatory role in cell fate transitions targeting a broad spectrum of functions. Network structure suggests DEK1-gated sequential transition between cell fates in 2D to 3D development. We anticipate that both our method combining phenotyping, transcriptomics and data science to dissect phenotypic traits and our model explaining the calpain’s role as a switch gatekeeping cell fate transitions will inform biology beyond plant development.

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