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

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 The microRNAs let-7 and miR-278 regulate insect metamorphosis and oogenesis by targeting the juvenile hormone early-response gene Krüppel-homolog 1

Development ◽  
2018 ◽  
Vol 145 (24) ◽  
pp. dev170670 ◽  
Author(s):  
Jiasheng Song ◽  
Wanwan Li ◽  
Haihong Zhao ◽  
Lulu Gao ◽  
Yuning Fan ◽  
...  
Keyword(s):  
Juvenile Hormone ◽  
Early Response ◽  
Response Gene ◽  
Early Response Gene ◽  
Insect Metamorphosis ◽  
Krüppel Homolog 1

scholarly journals Molecular mechanism underlying juvenile hormone-mediated repression of precocious larval–adult metamorphosis

2017 ◽  
Vol 114 (5) ◽  
pp. 1057-1062 ◽  
Author(s):  
Takumi Kayukawa ◽  
Akiya Jouraku ◽  
Yuka Ito ◽  
Tetsuro Shinoda
Keyword(s):  
Juvenile Hormone ◽  
Cell Line ◽  
Adult Development ◽  
Transcriptional Repression ◽  
Molecular Mechanisms ◽  
Pupal Stage ◽  
Genetic Network ◽  
Holometabolous Insect ◽  
Insect Metamorphosis ◽  
Krüppel Homolog 1

Juvenile hormone (JH) represses precocious metamorphosis of larval to pupal and adult transitions in holometabolous insects. The early JH-inducible geneKrüppel homolog 1(Kr-h1) plays a key role in the repression of metamorphosis as a mediator of JH action. Previous studies demonstrated that Kr-h1 inhibits precocious larval–pupal transition in immature larva via direct transcriptional repression of the pupal specifierBroad-Complex(BR-C). JH was recently reported to repress the adult specifier geneEcdysone-induced protein 93F(E93); however, its mechanism of action remains unclear. Here, we found that JH suppressed ecdysone-inducibleE93expression in the epidermis of the silkwormBombyx moriand in aB. moricell line. Reporter assays in the cell line revealed that the JH-dependent suppression was mediated by Kr-h1. Genome-wide ChIP-seq analysis identified a consensus Kr-h1 binding site (KBS, 14 bp) located in theE93promoter region, and EMSA confirmed that Kr-h1 directly binds to the KBS. Moreover, we identified a C-terminal conserved domain in Kr-h1 essential for the transcriptional repression ofE93. Based on these results, we propose a mechanism in which JH-inducible Kr-h1 directly binds to the KBS site upstream of theE93locus to repress its transcription in a cell-autonomous manner, thereby preventing larva from bypassing the pupal stage and progressing to precocious adult development. These findings help to elucidate the molecular mechanisms regulating the metamorphic genetic network, including the functional significance ofKr-h1,BR-C, andE93in holometabolous insect metamorphosis.

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.

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