scholarly journals Expression of Novel ING Variants Is Regulated by Thyroid Hormone in theXenopus laevisTadpole

2001 ◽  
Vol 276 (50) ◽  
pp. 47013-47020 ◽  
Author(s):  
Mary J. Wagner ◽  
Markéta Gogela-Spehar ◽  
Rachel C. Skirrow ◽  
Randal N. Johnston ◽  
Karl Riabowol ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Thyroid Hormone ◽  
Cell Fate ◽  
Splice Variants ◽  
Family Members ◽  
Specific Pattern ◽  
Protein Isoforms ◽  
Modulate Function ◽  
Western Blots ◽  
Tissue Specific

The candidate tumor suppressor gene,ING1, encodes several protein isoforms as a result of alternative splicing that may possess agonistic and antagonistic roles in the control of cell proliferation and apoptosis. Recently a related gene,ING2, was isolated in human whose expression is increased in adenocarcinomas. Little is known about the cellular function and regulation of these ING family members, but the fact that ING proteins contain a plant homeodomain finger suggests that these proteins may modulate transcription factor-mediated pathways. To elucidate how ING may interact in different tissues to modulate function, we used amphibian metamorphosis as a model system in which a single stimulus, thyroid hormone (TH), initiates tissue-specific proliferation, differentiation, and apoptosis. We have isolated the firstXenopus laevis ING2and demonstrate that transcript levels increase in response to TH treatment. We provide evidence for the existence of splice variants that are differentially expressed in tissues with different TH-induced fates. Western blots using an antibody directed against the highly conserved C-terminal end of ING proteins reveal a tissue-specific pattern of ING isoform expression in adultXenopustissues. Analyses of premetamorphic tadpole tissues show a TH-induced accumulation of ING proteins in tail, whereas the levels in the leg are not affected. This TH-induced accumulation is also observed in serum-free tail organ cultures and is prevented by inhibitors of tail apoptosis. Therefore, this work presents the first link between ING expression and a hormonally regulated nuclear transcription factor-mediated apoptotic response opening the possibility that ING family members may be involved in transducing the signal initiated by TH that determines cell fate.

scholarly journals Reciprocal cross-regulation of VND and SND multigene TF families for wood formation in Populus trichocarpa

2017 ◽  
Vol 114 (45) ◽  
pp. E9722-E9729 ◽  
Author(s):  
Ying-Chung Jimmy Lin ◽  
Hao Chen ◽  
Quanzi Li ◽  
Wei Li ◽  
Jack P. Wang ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Transcription Factors ◽  
Splice Variant ◽  
Reciprocal Cross ◽  
Splice Variants ◽  
Family Members ◽  
Wood Formation ◽  
Negative Regulator ◽  
General Mechanism ◽  
Nac Domain

Secondary cell wall (SCW) biosynthesis is the biological process that generates wood, an important renewable feedstock for materials and energy. NAC domain transcription factors, particularly Vascular-Related NAC-Domain (VND) and Secondary Wall-Associated NAC Domain (SND) proteins, are known to regulate SCW differentiation. The regulation of VND and SND is important to maintain homeostasis for plants to avoid abnormal growth and development. We previously identified a splice variant, PtrSND1-A2IR, derived from PtrSND1-A2 as a dominant-negative regulator, which suppresses the transactivation of all PtrSND1 family members. PtrSND1-A2IR also suppresses the self-activation of the PtrSND1 family members except for its cognate transcription factor, PtrSND1-A2, suggesting the existence of an unknown factor needed to regulate PtrSND1-A2. Here, a splice variant, PtrVND6-C1IR, derived from PtrVND6-C1 was discovered that suppresses the protein functions of all PtrVND6 family members. PtrVND6-C1IR also suppresses the expression of all PtrSND1 members, including PtrSND1-A2, demonstrating that PtrVND6-C1IR is the previously unidentified regulator of PtrSND1-A2. We also found that PtrVND6-C1IR cannot suppress the expression of its cognate transcription factor, PtrVND6-C1. PtrVND6-C1 is suppressed by PtrSND1-A2IR. Both PtrVND6-C1IR and PtrSND1-A2IR cannot suppress their cognate transcription factors but can suppress all members of the other family. The results indicate that the splice variants from the PtrVND6 and PtrSND1 family may exert reciprocal cross-regulation for complete transcriptional regulation of these two families in wood formation. This reciprocal cross-regulation between families suggests a general mechanism among NAC domain proteins and likely other transcription factors, where intron-retained splice variants provide an additional level of regulation.

The role of p63 in epidermal morphogenesis and neoplasia

2010 ◽  
Vol 38 (1) ◽  
pp. 223-228 ◽  
Author(s):  
Simon S. McDade ◽  
Dennis J. McCance
Keyword(s):  
Transcription Factors ◽  
Splice Variants ◽  
Family Members ◽  
Protein Isoforms ◽  
Structural Homology ◽  
P53 Family ◽  
Multiple Protein ◽  
Proliferation And Differentiation ◽  
Epidermal Morphogenesis

The p53 family of transcription factors is made up of p53, p63 and p73, which share significant structural homology. In particular, transcriptional complexity and the expression of multiple protein isoforms are an emergent trait of all family members. p63 is the evolutionarily eldest member of the p53 family and the various isoforms have critical roles in the development of stratifying epithelia. Recent results have uncovered additional splice variants, adding to the complexity of the transcriptional architecture of p63. These observations and the emerging extensive interplay between p63 and p53 in development, proliferation and differentiation underline the importance of considering all isoforms and family members in studies of the function of p53 family members.

scholarly journals Interactions between Hairy/Enhancer of Split-related proteins and the pancreatic transcription factor Ptf1-p48 modulate function of the PTF1 transcriptional complex

2006 ◽  
Vol 393 (3) ◽  
pp. 679-685 ◽  
Author(s):  
Bidyut Ghosh ◽  
Steven D. Leach
Keyword(s):  
Transcription Factor ◽  
Family Members ◽  
Direct Interaction ◽  
Inhibitory Effect ◽  
Effector Proteins ◽  
Glutathione S Transferase ◽  
Modulate Function ◽  
Helix Loop Helix ◽  
Transcriptional Complex ◽  
Enhancer Of Split

In the developing pancreas, the onset of exocrine differentiation is driven by the activity of the PTF1 (pancreas transciption factor 1) transcriptional complex, which is comprised of the class II bHLH (basic helix–loop–helix) protein, Ptf1-p48 [also known as Ptf1a (pancreas specific transcription factor 1a)], and a class I E-box binding partner. Activity of the PTF1 complex is normally inhibited by the Notch signalling pathway, a process mediated by Notch effector proteins in the HES (Hairy/Enhancer of Split) family of bHLH transcriptional repressors. In the present study, we show that this inhibitory effect occurs through direct interaction between HES family members and Ptf1-p48. The HES family members Hey1 (hairy/enhancer-of-split related with YRPW motif 1) and Hey2 co-immunoprecipitate with Ptf1-p48, and Ptf1-p48 binding by Hes1 is also evident in yeast two-hybrid and GST (glutathione S-transferase) pull-down assays. The ability of Hes1 to interact with Ptf1-p48 resides within a fragment comprised of the bHLH, Orange and C-terminal domains, and does not require the N-terminal or WRPW elements. The ability of truncated versions of Hes1 to bind Ptf1-p48 correlates with their ability to down-regulate the activity of the PTF1 transcriptional complex, defining Ptf1-p48 binding as the most likely mechanism by which Notch effector proteins delay exocrine pancreatic differentiation.

scholarly journals Single-cell analysis of cell fate bifurcation in the chordate Ciona

BMC Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Konner M. Winkley ◽  
Wendy M. Reeves ◽  
Michael T. Veeman
Keyword(s):  
Transcription Factor ◽  
Cell Fate ◽  
Enrichment Analysis ◽  
Cell Types ◽  
Mapk Signaling ◽  
Embryonic Cell ◽  
Regulatory State ◽  
Cell Stage ◽  
Tissue Specific ◽  
Neural Lineage

Abstract Background Inductive signaling interactions between different cell types are a major mechanism for the further diversification of embryonic cell fates. Most blastomeres in the model chordate Ciona robusta become restricted to a single predominant fate between the 64-cell and mid-gastrula stages. The deeply stereotyped and well-characterized Ciona embryonic cell lineages allow the transcriptomic analysis of newly established cell types very early in their divergence from sibling cell states without the pseudotime inference needed in the analysis of less synchronized cell populations. This is the first ascidian study to use droplet scRNAseq with large numbers of analyzed cells as early as the 64-cell stage when major lineages such as primary notochord first become fate restricted. Results and conclusions We identify 59 distinct cell states, including new subregions of the b-line neural lineage and the early induction of the tail tip epidermis. We find that 34 of these cell states are directly or indirectly dependent on MAPK-mediated signaling critical to early Ciona patterning. Most of the MAPK-dependent bifurcations are canalized with the signal-induced cell fate lost upon MAPK inhibition, but the posterior endoderm is unique in being transformed into a novel state expressing some but not all markers of both endoderm and muscle. Divergent gene expression between newly bifurcated sibling cell types is dominated by upregulation in the induced cell type. The Ets family transcription factor Elk1/3/4 is uniquely upregulated in nearly all the putatively direct inductions. Elk1/3/4 upregulation together with Ets transcription factor binding site enrichment analysis enables inferences about which bifurcations are directly versus indirectly controlled by MAPK signaling. We examine notochord induction in detail and find that the transition between a Zic/Ets-mediated regulatory state and a Brachyury/FoxA-mediated regulatory state is unexpectedly late. This supports a “broad-hourglass” model of cell fate specification in which many early tissue-specific genes are induced in parallel to key tissue-specific transcriptional regulators via the same set of transcriptional inputs.

scholarly journals HNF4beta, a new gene of the HNF4 family with distinct activation and expression profiles in oogenesis and embryogenesis of Xenopus laevis.

1997 ◽  
Vol 17 (2) ◽  
pp. 687-694 ◽  
Author(s):  
B Holewa ◽  
D Zapp ◽  
T Drewes ◽  
S Senkel ◽  
G U Ryffel
Keyword(s):  
Transcription Factor ◽  
Reverse Transcription ◽  
Splice Variants ◽  
Expression Profiles ◽  
Rna Stability ◽  
Tail Bud ◽  
Tissue Specific ◽  
Specific Transcription Factor ◽  
Reverse Transcription Pcr ◽  
New Gene

The transcription factor hepatocyte nuclear factor 4 (HNF4) is an orphan member of the nuclear receptor superfamily expressed in mammals in liver, kidney, and the digestive tract. Recently, we isolated the Xenopus homolog of mammalian HNF4 and revealed that it is not only a tissue-specific transcription factor but also a maternal component of the Xenopus egg and distributed within an animal-to-vegetal gradient. We speculate that this gradient cooperates with the vegetally localized embryonic induction factor activin A to activate expression of HNF1alpha, a tissue-specific transcription factor with an expression pattern overlapping that of HNF4. We have now identified a second Xenopus HNF4 gene, which is more distantly related to mammalian HNF4 than the previously isolated gene. This new gene was named HNF4beta to distinguish it from the known HNF4 gene, which is now called HNF4alpha. By reverse transcription-PCR, we detected within the 5' untranslated region of HNF4beta two splice variants (HNF4beta2 and HNF4beta3) with additional exons, which seem to affect RNA stability. HNF4beta is a functional transcription factor acting sequence specifically on HNF4 binding sites known for HNF4alpha, but it seems to have a lower DNA binding activity and is a weaker transactivator than the alpha isoform. Furthermore, the two factors differ with respect to tissue distribution in adult frogs: whereas HNF4alpha is expressed in liver and kidney, HNF4beta is expressed in addition in stomach, intestine, lung, ovary, and testis. Both factors are maternal proteins and present at constant levels throughout embryogenesis. However, using reverse transcription-PCR, we found the RNA levels to change substantially: whereas HNF4alpha is expressed early during oogenesis and is absent in the egg, HNF4beta is first detected in the latest stage of oogenesis, and transcripts are present in the egg and early cleavage stages. Furthermore, zygotic HNF4alpha transcripts appear in early gastrula and accumulate during further embryogenesis, whereas HNF4beta mRNA transiently appears during gastrulation before it accumulates again at the tail bud stage. All of these distinct characteristics of the newly identified HNF4 protein imply that the alpha and beta isoform have different functions in development and in adult tissues.

scholarly journals The EGL-13 SOX Domain Transcription Factor Affects the Uterine Cell Lineages in Caenorhabditis elegans

Genetics ◽  
2003 ◽  
Vol 165 (3) ◽  
pp. 1623-1628
Author(s):  
Hediye Nese Cinar ◽  
Keri L Richards ◽  
Kavita S Oommen ◽  
Anna P Newman
Keyword(s):  
Transcription Factor ◽  
Cell Division ◽  
Caenorhabditis Elegans ◽  
Cell Fate ◽  
Cell Lineages

Abstract We isolated egl-13 mutants in which the cells of the Caenorhabditis elegans uterus initially appeared to develop normally but then underwent an extra round of cell division. The data suggest that egl-13 is required for maintenance of the cell fate.

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