scholarly journals Gamete fusion rapidly reconstitutes a bi-partite transcription factor to block re-fertilization

2018 ◽  
Author(s):  
Aleksandar Vještica ◽  
Laura Merlini ◽  
Pedro N’kosi ◽  
Sophie G Martin
Keyword(s):  
Transcription Factor ◽  
Sexual Reproduction ◽  
Model Organism ◽  
Nuclear Accumulation ◽  
M Cell ◽  
Cell Fates ◽  
Gamete Fusion ◽  
Zygotic Transcription ◽  
Distinct Cell ◽  
Homeobox Protein

AbstractThe ploidy cycle, integral to sexual reproduction, requires not only meiosis to halve the number of chromosomes, but also mechanisms that ensure zygotes are formed by exactly two partners1–5. During sexual reproduction of the fungal model organism Schizosaccharomyces pombe, haploid P- and M-cells normally fuse to form a diploid zygote that immediately enters meiosis6. Here, we reveal that fast post-fusion reconstitution of a bi-partite transcription factor actively blocks re-fertilization. We first identify mutants that undergo transient cell fusion involving cytosol exchange but not karyogamy, and show this drives distinct cell fates in the two gametes: The P-partner undergoes lethal, haploid meiosis while the M-cell persists in mating. Consistently, we find that the zygotic transcription that drives meiosis is initiated rapidly only from the P-parental genome, even in wild type cells. This asymmetric gene expression depends on a bi-partite complex formed post-fusion between the nuclear P-cell-specific homeobox protein Pi and a cytosolic M-specific peptide Mi7,8, which is captured by Pi in the P-nucleus. Zygotic transcription is thus poised to initiate in the P-nucleus as fast as Mi reaches it. The asymmetric nuclear accumulation is inherent to the transcription factor design, and is reconstituted by a pair of synthetic interactors, one localized to the nucleus of one gamete and the other in the cytosol of its partner. Strikingly, imposing a delay in zygotic transcription, by postponing Mi expression or deleting its transcriptional target in the P-genome, leads to zygotes fusing with additional gametes, thus forming polyploids and eventually aneuploid progeny. We further show that the signaling cascade to block re-fertilization shares components with, but bifurcates from, meiotic induction9–11. Thus, cytoplasmic connection upon gamete fusion leads to rapid reconstitution of a bi-partite transcription factor in one partner to block re-fertilization and induce meiosis, thus ensuring genome maintenance during sexual reproduction.

scholarly journals Transcriptional dynamics of gametogenesis in the green seaweed Ulva mutabilis identifies an RWP-RK transcription factor linked to reproduction

2022 ◽  
Vol 22 (1) ◽  
Author(s):  
Xiaojie Liu ◽  
Jonas Blomme ◽  
Kenny A. Bogaert ◽  
Sofie D’hondt ◽  
Thomas Wichard ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Sexual Reproduction ◽  
Higher Plants ◽  
Crop Improvement ◽  
Functional Characterization ◽  
Model Organism ◽  
Land Plants ◽  
Alternative Source ◽  
Starting Point ◽  
Green Seaweed

Abstract Background The molecular mechanism underlying sexual reproduction in land plants is well understood in model plants and is a target for crop improvement. However, unlike land plants, the genetic basis involved in triggering reproduction and gamete formation remains elusive in most seaweeds, which are increasingly viewed as an alternative source of functional food and feedstock for energy applications. Results Gametogenesis of Ulva mutabilis, a model organism for green seaweeds, was studied. We analyzed transcriptome dynamics at different time points during gametogenesis following induction of reproduction by fragmentation and removal of sporulation inhibitors. Analyses demonstrated that 45% of the genes in the genome were differentially expressed during gametogenesis. We identified several transcription factors that potentially play a key role in the early gametogenesis of Ulva given the function of their homologs in higher plants and microalgae. In particular, the detailed expression pattern of an evolutionarily conserved transcription factor containing an RWP-RK domain suggested a key role during Ulva gametogenesis. Conclusions Transcriptomic analyses of gametogenesis in the green seaweed Ulva highlight the importance of a conserved RWP-RK transcription factor in the induction of sexual reproduction. The identification of putative master regulators of gametogenesis provides a starting point for further functional characterization.

Mezzo, apaired-likehomeobox protein is an immediate target of Nodal signalling and regulates endoderm specification in zebrafish

Development ◽  
2002 ◽  
Vol 129 (21) ◽  
pp. 4901-4914 ◽  
Author(s):  
Morgane Poulain ◽  
Thierry Lepage
Keyword(s):  
Transcription Factor ◽  
Marker Gene ◽  
Ectopic Expression ◽  
Signalling Pathway ◽  
Turn On ◽  
Zygotic Transcription ◽  
Homeobox Protein ◽  
Morpholino Oligonucleotides ◽  
Antisense Morpholino Oligonucleotides ◽  
Antisense Morpholino

Endoderm specification in zebrafish is mediated by the zygotic transcription factors Bon/Mixer, Faust/Gata5, Casanova and Sox17, whose expression is induced by Nodal signalling. Bon/Mixer and Gata5 require Casanova in order to promote endoderm formation and all three factors act upstream of sox17, but it is not clear whether Casanova acts downstream of or in parallel to Bon/Mixer and Gata5. An additional factor induced at the margin of the blastoderm by Nodal signalling is thought to be required to induce casanova expression. We show that Mezzo, a novelpaired-like homeobox protein, may be this missing transcription factor. The homeobox of Mezzo is mostly related to the homeodomain of the Mix-like and Mixer homeoproteins, but Mezzo is distinct from Bon/Mixer, the product of the bonnie and clyde gene. Like bon/mixer, mezzois expressed transiently in mesendoderm precursors. By analysing the expression of mezzo in various mutants of Nodal signalling, we show that its expression strictly depends on a functional Nodal signalling pathway. By expressing a constitutively active Nodal receptor in the presence of translation inhibitors, we further demonstrate that mezzo, bonnie and clyde, and casanova are all immediate early targets of Nodal signalling, while sox17 requires post-MBT protein synthesis in order to be induced. Overexpression of mezzo mRNA can induce ectopic expression of casanova and sox17 and can also turn on the pan mesodermal marker gene ntl. We show that the function ofmezzo is redundant with that of bonnie and clyde and thatmezzo RNA can partially rescue bonnie and clyde mutants. Injection of antisense Morpholino oligonucleotides targeted againstmezzo into bonnie and clyde mutant embryos abolishes allsox17 expression and aggravates their mutant phenotype. These results highlight the complexity of the transcriptional network operating during endoderm formation. They place mezzo as a new transcription factor with unique properties acting in parallel with bonnie and clyde,faust and casanova in the Nodal signalling pathway that controls specification of mesoderm and endoderm in zebrafish.

Rabbit M cells and dome enterocytes are distinct cell lineages

2001 ◽  
Vol 114 (11) ◽  
pp. 2077-2083
Author(s):  
Hugues Lelouard ◽  
Alain Sahuquet ◽  
Hubert Reggio ◽  
Philippe Montcourrier
Keyword(s):  
Lymphoid Tissues ◽  
M Cells ◽  
Relative Distribution ◽  
M Cell ◽  
Epithelial Surface ◽  
Cell Lineages ◽  
Proliferative Zone ◽  
Early Appearance ◽  
Distinct Cell ◽  
Constant Distribution

We have studied the M cell origin and differentiation pathway in rabbit gut-associated lymphoid tissues. Micro-dissected domes and epithelium isolated by ethylene diamine tetra acetic acid detachment allowed us to view the whole epithelial surface from the bottom of crypts to the top of domes. We used monoclonal antibodies specific to the apex of either M cells or dome enterocytes, lectins, and antibodies to vimentin in appendix, distal Peyer’s patches and caecal patches. The earliest vimentin-labeled M cells were observed in the BrdU-positive proliferative zone of dome-associated crypts. Gradual differentiation of the M cell vimentin cytoskeleton started at this site to progressively give rise to the first pocket-forming M cells in the upper dome. Therefore, these mitotic cells of the crypts appear as the direct precursors of M cells. In addition to an early appearance of M cell markers, a regular mosaic-like relative distribution of M cells and dome enterocytes was already detected in the vicinity of crypts, similar to that observed on the lateral surface of domes where functional M cells lie. This constant distribution implies that there is no trans-differentiation of enterocytes to M cells along the crypt-dome axis. Together, these observations provide very strong evidence in favor of an early commitment in crypts of M cell and enterocyte distinct lineages.

GHF-1, a Tissue-Specific Transcription Factor, is a Homeobox Protein

1989 ◽  
pp. 90-109
Author(s):  
José-Luis Castrillo ◽  
Lars E. Theill ◽  
Mordechai Bodner ◽  
Michael Karin
Keyword(s):  
Transcription Factor ◽  
Tissue Specific ◽  
Specific Transcription Factor ◽  
Homeobox Protein

Xenopus nuclear factor 7 (xnf7) possesses an NLS that functions efficiently in both oocytes and embryos

1993 ◽  
Vol 105 (2) ◽  
pp. 389-395
Author(s):  
X. Li ◽  
L.D. Etkin
Keyword(s):  
Transcription Factor ◽  
Zinc Finger ◽  
Nuclear Localization ◽  
Nuclear Localization Signal ◽  
Nuclear Accumulation ◽  
Nuclear Factor ◽  
Zinc Finger Gene ◽  
Early Embryos ◽  
Localization Signal ◽  
Nuclear Phosphoprotein

Xenopus nuclear factor 7 (xnf7) is a nuclear phosphoprotein that is encoded by a member of a novel zinc finger gene family and likely functions as a transcription factor. It possesses a nuclear localization signal (NLS) similar to the bipartite basic NLS of nucleoplasmin, but unlike nucleoplasmin, which re-enters nuclei immediately after fertilization, xnf7 remains cytoplasmic until the mid-blastula transition (MBT). We have measured the accumulation of injected labeled xnf7 protein or protein produced from synthetic xnf7 transcripts in the oocyte nuclei (GV). The data show that the NLS of xnf7 functions efficiently in oocytes. Mutations in either of the bipartite basic domains of the xnf7 NLS inhibit nuclear accumulation, while mutations in the spacer sequences have no effect. The xnf7 NLS linked to pyruvate kinase directs the efficient accumulation of this protein into nuclei of early embryos prior to the MBT. These data suggest that retention of the xnf7 protein during development is the result of a mechanism that interferes with the xnf7 NLS function.

scholarly journals Persistent NF-κB activation in renal epithelial cells in a mouse model of HIV-associated nephropathy

2006 ◽  
Vol 290 (3) ◽  
pp. F657-F665 ◽  
Author(s):  
Scott Martinka ◽  
Leslie A. Bruggeman
Keyword(s):  
Transcription Factor ◽  
Epithelial Cells ◽  
Cell Types ◽  
Nuclear Accumulation ◽  
Mobility Shift ◽  
Glomerular Epithelial Cells ◽  
Host Virus Interactions ◽  
Virus Interactions ◽  
Electrophoretic Mobility Shift Assays ◽  
Hiv 1

Human immunodeficiency virus (HIV)-associated nephropathy (HIVAN) is caused, in part, by direct infection of kidney epithelial cells by HIV-1. In the spectrum of pathogenic host-virus interactions, abnormal activation or suppression of host transcription factors is common. NF-κB is a necessary host transcription factor for HIV-1 gene expression, and it has been shown that NF-κB activity is dysregulated in many naturally infected cell types. We show here that renal glomerular epithelial cells (podocytes) expressing the HIV-1 genome, similar to infected immune cells, also have a dysregulated and persistent activation of NF-κB. Although podocytes produce p50, p52, RelA, RelB, and c-Rel, electrophoretic mobility shift assays and immunocytochemistry showed a predominant nuclear accumulation of p50/RelA-containing NF-κB dimers in HIV-1-expressing podocytes compared with normal. In addition, the expression level of a transfected NF-κB reporter plasmid was significantly higher in HIVAN podocytes. The mechanism of NF-κB activation involved increased phosphorylation of IκBα, resulting in an enhanced turnover of the IκBα protein. There was no evidence for regulation by IκBβ or the alternate pathway of NF-κB activation. Altered activation of this key host transcription factor likely plays a role in the well-described cellular phenotypic changes observed in HIVAN, such as proliferation. Studies with inhibitors of proliferation and NF-κB suggest that NF-κB activation may contribute to the proliferative mechanism in HIVAN. In addition, because NF-κB regulates many aspects of inflammation, this dysregulation may also contribute to disease severity and progression through regulation of proinflammatory processes in the kidney microenvironment.

Sign in / Sign up

Export Citation Format

Share Document