scholarly journals MiR-2 family regulates insect metamorphosis by controlling the juvenile hormone signaling pathway

2015 ◽  
Vol 112 (12) ◽  
pp. 3740-3745 ◽  
Author(s):  
Jesus Lozano ◽  
Raúl Montañez ◽  
Xavier Belles
Keyword(s):  
Transcription Factor ◽  
Juvenile Hormone ◽  
Binding Site ◽  
Signaling Pathway ◽  
Blattella Germanica ◽  
Mrna Levels ◽  
Hormone Signaling ◽  
Nymphal Instar ◽  
Insect Metamorphosis ◽  
Krüppel Homolog 1

In 2009 we reported that depletion of Dicer-1, the enzyme that catalyzes the final step of miRNA biosynthesis, prevents metamorphosis inBlattella germanica. However, the precise regulatory roles of miRNAs in the process have remained elusive. In the present work, we have observed that Dicer-1 depletion results in an increase of mRNA levels of Krüppel homolog 1 (Kr-h1), a juvenile hormone-dependent transcription factor that represses metamorphosis, and that depletion of Kr-h1 expression in Dicer-1 knockdown individuals rescues metamorphosis. We have also found that the 3′UTR of Kr-h1 mRNA contains a functional binding site for miR-2 family miRNAs (for miR-2, miR-13a, and miR-13b). These data suggest that metamorphosis impairment caused by Dicer-1 and miRNA depletion is due to a deregulation of Kr-h1 expression and that this deregulation is derived from a deficiency of miR-2 miRNAs. We corroborated this by treating the last nymphal instar ofB. germanicawith an miR-2 inhibitor, which impaired metamorphosis, and by treating Dicer-1-depleted individuals with an miR-2 mimic to allow nymphal-to-adult metamorphosis to proceed. Taken together, the data indicate that miR-2 miRNAs scavenge Kr-h1 transcripts when the transition from nymph to adult should be taking place, thus crucially contributing to the correct culmination of metamorphosis.

scholarly journals Myoglianin triggers the pre-metamorphosis stage in hemimetabolan insects

2018 ◽  
Author(s):  
Orathai Kamsoi ◽  
Xavier Belles
Keyword(s):  
Cell Proliferation ◽  
Juvenile Hormone ◽  
Signaling Pathway ◽  
Corpora Allata ◽  
Nymphal Instar ◽  
Relevant Question ◽  
Prothoracic Glands ◽  
Biosynthesis Gene ◽  
Insect Metamorphosis ◽  
Juvenile Instar

ABSTRACTInsect metamorphosis is triggered by a decrease in juvenile hormone (JH) in the final juvenile instar. What induces this decline is therefore a very relevant question. Working with the cockroach Blattella germanica, we found that Myoglianin (Myo), a ligand in the TGF-β signaling pathway, is highly expressed in the corpora allata (CA, the JH producing glands) and prothoracic glands (PG, which produce ecdysone) during the penultimate nymphal instar (N5). In the CA, high Myo levels during N5 repress the expression of jhamt, a JH biosynthesis gene. In the PG, decreasing JH levels trigger gland degeneration, mediated by the factors Kr-h1, FTZ-F1, E93 and IAP1. Also in the PG, a peak of myo expression in N5 stimulates the expression of ecdysone biosynthesis genes, such as nvd, thus enhancing the production of the metamorphic ecdysone pulse in N6. The myo expression peak in N5 also represses cell proliferation, which can contribute to enhance ecdysone production. The data indicate that Myo triggers the pre-metamorphic nymphal instar in B. germanica, and possibly in other hemimetabolan insects.

scholarly journals Characterization of E93 in neometabolous thrips Frankliniella occidentalis and Haplothrips brevitubus

PLoS ONE ◽  
2021 ◽  
Vol 16 (7) ◽  
pp. e0254963
Author(s):  
Youhei Suzuki ◽  
Takahiro Shiotsuki ◽  
Akiya Jouraku ◽  
Ken Miura ◽  
Chieka Minakuchi
Keyword(s):  
Larval Stage ◽  
Hormonal Regulation ◽  
Frankliniella Occidentalis ◽  
Expression Profiles ◽  
Mrna Levels ◽  
Transcript Levels ◽  
Adult Transition ◽  
Thrips Species ◽  
Insect Metamorphosis ◽  
Krüppel Homolog 1

Insect metamorphosis into an adult occurs after the juvenile hormone (JH) titer decreases at the end of the juvenile stage. This generally coincides with decreased transcript levels of JH-response transcription factors Krüppel homolog 1 (Kr-h1) and broad (br), and increased transcript levels of the adult specifier E93. Thrips (Thysanoptera) develop through inactive and non-feeding stages referred to as “propupa” and “pupa”, and this type of distinctive metamorphosis is called neometaboly. To understand the mechanisms of hormonal regulation in thrips metamorphosis, we previously analyzed the transcript levels of Kr-h1 and br in two thrips species, Frankliniella occidentalis (Thripidae) and Haplothrips brevitubus (Phlaeothripidae). In both species, the transcript levels of Kr-h1 and br decreased in the “propupal” and “pupal” stages, and their transcription was upregulated by exogenous JH mimic treatment. Here we analyzed the developmental profiles of E93 in these two thrips species. Quantitative RT-PCR revealed that E93 expression started to increase at the end of the larval stage in F. occidentalis and in the “propupal” stage of H. brevitubus, as Kr-h1 and br mRNA levels decreased. Treatment with an exogenous JH mimic at the onset of metamorphosis prevented pupal-adult transition and caused repression of E93. These results indicated that E93 is involved in adult differentiation after JH titer decreases at the end of the larval stage of thrips. By comparing the expression profiles of Kr-h1, br, and E93 among insect species, we propose that the “propupal” and “pupal” stages of thrips have some similarities with the holometabolous prepupal and pupal stages, respectively.

scholarly journals Transcriptional regulation of juvenile hormone-mediated induction of Kruppel homolog 1, a repressor of insect metamorphosis

2012 ◽  
Vol 109 (29) ◽  
pp. 11729-11734 ◽  
Author(s):  
T. Kayukawa ◽  
C. Minakuchi ◽  
T. Namiki ◽  
T. Togawa ◽  
M. Yoshiyama ◽  
...  
Keyword(s):  
Transcriptional Regulation ◽  
Juvenile Hormone ◽  
Insect Metamorphosis ◽  
Krüppel Homolog 1

The transcription factor Krüppel homolog 1 is linked to the juvenile hormone-dependent maturation of sexual behavior in the male moth, Agrotis ipsilon

2012 ◽  
Vol 176 (2) ◽  
pp. 158-166 ◽  
Author(s):  
Line Duportets ◽  
Françoise Bozzolan ◽  
Antoine Abrieux ◽  
Annick Maria ◽  
Christophe Gadenne ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Sexual Behavior ◽  
Juvenile Hormone ◽  
Agrotis Ipsilon ◽  
Male Moth ◽  
Krüppel Homolog 1

ZFP143 Activates C/EBPα Transcription in Myeloid Cells.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 1233-1233
Author(s):  
Boris Bartholdy ◽  
David Gonzalez ◽  
Daniel G. Tenen
Keyword(s):  
Transcription Factor ◽  
Binding Site ◽  
Blast Crisis ◽  
Myeloid Cells ◽  
Gene Trap ◽  
Myelogenous Leukemia ◽  
Mrna Levels ◽  
Consensus Binding Site ◽  
Differentiation Block

Abstract C/EBPα is a key transcription factor involved in myeloid differentiation and frequently mutated or deregulated in human acute myeloid leukemias (AML) as well as in blast crisis of chronic myelogenous leukemia (CML). Disruption of its function contributes to the differentiation block observed in these diseases and thus to leukemogenesis. Here, we have identified a conserved region in the C/EBPα promoter that is important for activation of C/EBPα transcription in myeloid cells and narrowed it down to a conserved site of approximately 25 bp that contains a consensus binding site for ZFP143, a seven-zinc finger transcription factor. In gel retardation assays, this region bound a factor of approximately 100 kDa that we biochemically purified and identified by mass spectrometry as being indeed ZFP143. In vivo binding of ZFP143 to its bona fide binding site in the C/EBPα promoter was also detected by chromatin immunoprecipitation assays. We are now studying the in vivo effect of ZFP143 on C/EBPα transcription in mice that carry an inducible gene trap in the ZFP143 locus. While mice homozygous for the active gene trap - that prevents ZFP143 transcription - die at an early embryonic stage, preliminary data from heterozygous mice shows indeed a reduction of C/EBPα mRNA levels, suggesting a role for ZFP143 in C/EBPα transcription activation. Ongoing experiments aim at selectively inactivating ZFP143 in the hematopoietic system using the Mx1-Cre / loxP system.

scholarly journals The MODY1 Gene for Hepatocyte Nuclear Factor 4α and a Feedback Loop Control COUP-TFII Expression in Pancreatic Beta Cells

2008 ◽  
Vol 28 (14) ◽  
pp. 4588-4597 ◽  
Author(s):  
Anaïs Perilhou ◽  
Cécile Tourrel-Cuzin ◽  
Pili Zhang ◽  
Ilham Kharroubi ◽  
Haiyan Wang ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Insulin Secretion ◽  
Binding Site ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Gene Promoter ◽  
Mrna Levels ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
Hepatocyte Nuclear Factor 4Α

ABSTRACT Pancreatic islet beta cell differentiation and function are dependent upon a group of transcription factors that maintain the expression of key genes and suppress others. Knockout mice with the heterozygous deletion of the gene for chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) or the complete disruption of the gene for hepatocyte nuclear factor 4α (HNF4α) in pancreatic beta cells have similar insulin secretion defects, leading us to hypothesize that there is transcriptional cross talk between these two nuclear receptors. Here, we demonstrate specific HNF4α activation of a reporter plasmid containing the COUP-TFII gene promoter region in transfected pancreatic beta cells. The stable association of the endogenous HNF4α with a region of the COUP-TFII gene promoter that contains a direct repeat 1 (DR-1) binding site was revealed by chromatin immunoprecipitation. Mutation experiments showed that this DR-1 site is essential for HNF4α transactivation of COUP-TFII. The dominant negative suppression of HNF4α function decreased endogenous COUP-TFII expression, and the specific inactivation of COUP-TFII by small interfering RNA caused HNF4α mRNA levels in 832/13 INS-1 cells to decrease. This positive regulation of HNF4α by COUP-TFII was confirmed by the adenovirus-mediated overexpression of human COUP-TFII (hCOUP-TFII), which increased HNF4α mRNA levels in 832/13 INS-1 cells and in mouse pancreatic islets. Finally, hCOUP-TFII overexpression showed that there is direct COUP-TFII autorepression, as COUP-TFII occupies the proximal DR-1 binding site of its own gene in vivo. Therefore, COUP-TFII may contribute to the control of insulin secretion through the complex HNF4α/maturity-onset diabetes of the young 1 (MODY1) transcription factor network operating in beta cells.

Bcl-2 Family Dysregulation in AML1-ETO-Expressing Human Hematopoietic Cells

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 5330-5330 ◽  
Author(s):  
Fu-Sheng Chou ◽  
Mark Wunderlich ◽  
James C. Mulloy
Keyword(s):  
Binding Site ◽  
Signaling Pathway ◽  
Chromosomal Translocation ◽  
Mrna Levels ◽  
Consensus Binding Site ◽  
Γ Irradiation ◽  
Hematopoietic Stem ◽  
P53 Signaling ◽  
P53 Activation ◽  
P53 Signaling Pathway

Abstract A subset of acute myeloid leukemia is caused by the chromosomal translocation (8;21), resulting in the expression of the AML1-ETO (AE) fusion protein. AE expression in human CD34+ umbilical cord blood (UCB) cells causes an expansion of the hematopoietic stem and progenitor cell (HSPC) compartment, but alone does not cause leukemia. We have recently shown that AE represses DNA damage repair genes, resulting in higher mutation frequency as well as p53 activation and increased basal apoptosis. Interestingly, we found that AE expression in CD34+ UCB cells was associated with high Bcl-xL levels, while control cells showed a gradual loss of Bcl-xL protein. Furthermore, expression of AE in aged HSPC that had already downregulated Bcl-xL also led to Bcl-xL protein upregulation. In addition, Bcl-xL protein, but not mRNA, was decreased by pharmacological and RNAi-mediated inhibition of p53 in AE cells and increased by low-intensity γ-irradiation, implying that Bcl-xL turnover may be post-translationally regulated by p53 levels. Bcl-xL knock-down by short-hairpin RNA in AE cells resulted in even higher p53 activity and growth disadvantage, suggesting that AE cells depend largely upon Bcl-xL for survival in the context of p53 activation. AE cells are also more sensitive than long-term cultured UCB cells to GX15-070, a BH3-mimetic drug that binds and inhibits all anti-apoptotic Bcl-2 family proteins. The sensitivity of AE cells to Bcl-xL inhibition and GX15-070 treatment may be due to upregulation of various pro-apoptotic Bcl-2 family proteins. Surprisingly, p53-upregulated modulator of apoptosis (PUMA) mRNA levels were decreased or remained unchanged in association with AE expression, even in the context of an upregulated p53 signaling pathway. Chromatin immunoprecipitation assay revealed that AE binds to and AML1 binding site in the putative promoter of PUMA, in a region distinct from the p53 consensus binding site. Indeed, PUMA expression is increased in response to γ-irradiation in cells expressing AE. This suggests that AE may directly repress PUMA gene expression, but does not prevent p53 binding. Taken together, our data indicate that AE expression may lead to re-establishment of a new balance between the pro-apoptotic signals conveyed by the activated p53 signaling pathway and the pro-survival signals, presumably Bcl-xL upregulation and PUMA repression, within the Bcl-2 family proteins to ensure cell survival and propagation.

scholarly journals E93-depleted adult insects preserve the prothoracic gland and molt again

Development ◽  
2020 ◽  
Vol 147 (22) ◽  
pp. dev190066
Author(s):  
Orathai Kamsoi ◽  
Xavier Belles
Keyword(s):  
Transcription Factor ◽  
Crucial Role ◽  
Middle Devonian ◽  
Adult Stage ◽  
Epidermal Cells ◽  
Prothoracic Gland ◽  
Molting Hormone ◽  
Nymphal Instar ◽  
Insect Metamorphosis ◽  
Final Molt

ABSTRACTInsect metamorphosis originated around the middle Devonian, associated with the innovation of the final molt; this occurs after histolysis of the prothoracic gland (PG; which produces the molting hormone) in the first days of adulthood. We previously hypothesized that transcription factor E93 is crucial in the emergence of metamorphosis, because it triggers metamorphosis in extant insects. This work on the cockroach Blattella germanica reveals that E93 also plays a crucial role in the histolysis of PG, which fits the above hypothesis. Previous studies have shown that the transcription factor FTZ-F1 is essential for PG histolysis. We have found that FTZ-F1 depletion towards the end of the final nymphal instar downregulates the expression of E93, whereas E93-depleted nymphs molt to adults that retain a functional PG. Interestingly, these adults are able to molt again, which is exceptional in insects. The study of insects able to molt again in the adult stage may reveal clues about how nymphal epidermal cells definitively become adult cells, and whether it is possible to reverse this process.

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