scholarly journals Cold-induced protein RBM3 orchestrates neurogenesis via modulating Yap mRNA stability in cold stress

2018 ◽  
Vol 217 (10) ◽  
pp. 3464-3479 ◽  
Author(s):  
Wenlong Xia ◽  
Libo Su ◽  
Jianwei Jiao
Keyword(s):  
Cold Stress ◽  
Brain Development ◽  
Binding Sites ◽  
Rna Binding ◽  
Binding Motif ◽  
Embryonic Brain ◽  
Pregnant Mice ◽  
Important Basis ◽  
The Brain ◽  
Embryonic Brain Development

In mammals, a constant body temperature is an important basis for maintaining life activities. Here, we show that when pregnant mice are subjected to cold stress, the expression of RBM3, a cold-induced protein, is increased in the embryonic brain. When RBM3 is knocked down or knocked out in cold stress, embryonic brain development is more seriously affected, exhibiting abnormal neuronal differentiation. By detecting the change in mRNA expression during maternal cold stress, we demonstrate that Yap and its downstream molecules are altered at the RNA level. By analyzing RNA-binding motif of RBM3, we find that there are seven binding sites in 3′UTR region of Yap1 mRNA. Mechanistically, RBM3 binds to Yap1-3′UTR, regulates its stability, and affects the expression of YAP1. RBM3 and YAP1 overexpression can partially rescue the brain development defect caused by RBM3 knockout in cold stress. Collectively, our data demonstrate that cold temperature affects brain development, and RBM3 acts as a key protective regulator in cold stress.

scholarly journals Equivalence of the fly orthodenticle gene and the human OTX genes in embryonic brain development of Drosophila

Development ◽  
1998 ◽  
Vol 125 (9) ◽  
pp. 1703-1710 ◽  
Author(s):  
S. Leuzinger ◽  
F. Hirth ◽  
D. Gerlich ◽  
D. Acampora ◽  
A. Simeone ◽  
...  
Keyword(s):  
Brain Development ◽  
Gene Family ◽  
Nerve Cord ◽  
Ventral Nerve Cord ◽  
Time Windows ◽  
Specific Gene ◽  
Embryonic Brain ◽  
Genetic Rescue ◽  
The Brain ◽  
Embryonic Brain Development

Members of the orthodenticle gene family are essential for embryonic brain development in animals as diverse as insects and mammals. In Drosophila, mutational inactivation of the orthodenticle gene results in deletions in anterior parts of the embryonic brain and in defects in the ventral nerve cord. In the mouse, targeted elimination of the homologous Otx2 or Otx1 genes causes defects in forebrain and/or midbrain development. To determine the morphogenetic properties and the extent of evolutionary conservation of the orthodenticle gene family in embryonic brain development, genetic rescue experiments were carried out in Drosophila. Ubiquitous overexpression of the orthodenticle gene rescues both the brain defects and the ventral nerve cord defects in orthodenticle mutant embryos; morphology and nervous system-specific gene expression are restored. Two different time windows exist for the rescue of the brain versus the ventral nerve cord. Ubiquitous overexpression of the human OTX1 or OTX2 genes also rescues the brain and ventral nerve cord phenotypes in orthodenticle mutant embryos; in the brain, the efficiency of morphological rescue is lower than that obtained with overexpression of orthodenticle. Overexpression of either orthodenticle or the human OTX gene homologs in the wild-type embryo results in ectopic neural structures. The rescue of highly complex brain structures in Drosophila by either fly or human orthodenticle gene homologs indicates that these genes are interchangeable between vertebrates and invertebrates and provides further evidence for an evolutionarily conserved role of the orthodenticle gene family in brain development.

Inductive patterning of the embryonic brain in Drosophila

Development ◽  
2002 ◽  
Vol 129 (9) ◽  
pp. 2121-2128
Author(s):  
Damon T. Page
Keyword(s):  
Brain Development ◽  
Common Ancestor ◽  
Last Common Ancestor ◽  
Embryonic Brain ◽  
Germ Layers ◽  
Brain Anomaly ◽  
Prechordal Plate ◽  
Foregut Endoderm ◽  
The Brain ◽  
Brain Patterning

In vertebrates (deuterostomes), brain patterning depends on signals from adjacent tissues. For example, holoprosencephaly, the most common brain anomaly in humans, results from defects in signaling between the embryonic prechordal plate (consisting of the dorsal foregut endoderm and mesoderm) and the brain. I have examined whether a similar mechanism of brain development occurs in the protostome Drosophila, and find that the foregut and mesoderm act to pattern the fly embryonic brain. When the foregut and mesoderm of Drosophila are ablated, brain patterning is disrupted. The loss of Hedgehog expressed in the foregut appears to mediate this effect, as it does in vertebrates. One mechanism whereby these defects occur is a disruption of normal apoptosis in the brain. These data argue that the last common ancestor of protostomes and deuterostomes had a prototype of the brains present in modern animals, and also suggest that the foregut and mesoderm contributed to the patterning of this ‘proto-brain’. They also argue that the foreguts of protostomes and deuterostomes, which have traditionally been assigned to different germ layers, are actually homologous.

Morphologic and neurochemical studies of embryonic brain development in murine trisomy 16

1984 ◽  
Vol 15 (2) ◽  
pp. 155-166 ◽  
Author(s):  
Harvey S. Singer ◽  
Michael Tiemeyer ◽  
John C. Hedreen ◽  
John Gearhart ◽  
Joseph T. Coyle
Keyword(s):  
Brain Development ◽  
Embryonic Brain ◽  
Trisomy 16 ◽  
Embryonic Brain Development

scholarly journals Identification of FMRP target mRNAs in the developmental brain: FMRP might coordinate Ras/MAPK, Wnt/β-catenin, and mTOR signaling during corticogenesis

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Cristine R. Casingal ◽  
Takako Kikkawa ◽  
Hitoshi Inada ◽  
Yukio Sasaki ◽  
Noriko Osumi
Keyword(s):  
Brain Development ◽  
Rna Binding ◽  
Fragile X ◽  
Autism Spectrum ◽  
Mtor Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Sequencing Analysis ◽  
Embryonic Brain ◽  
Target Mrnas ◽  
Mrna Targets

AbstractCorticogenesis is one of the most critical and complicated processes during embryonic brain development. Any slight impairment in corticogenesis could cause neurodevelopmental disorders such as Fragile X syndrome (FXS), of which symptoms contain intellectual disability (ID) and autism spectrum disorder (ASD). Fragile X mental retardation protein (FMRP), an RNA-binding protein responsible for FXS, shows strong expression in neural stem/precursor cells (NPCs) during corticogenesis, although its function during brain development remains largely unknown. In this study, we attempted to identify the FMRP target mRNAs in the cortical primordium using RNA immunoprecipitation sequencing analysis in the mouse embryonic brain. We identified 865 candidate genes as targets of FMRP involving 126 and 118 genes overlapped with ID and ASD-associated genes, respectively. These overlapped genes were enriched with those related to chromatin/chromosome organization and histone modifications, suggesting the involvement of FMRP in epigenetic regulation. We further identified a common set of 17 FMRP “core” target genes involved in neurogenesis/FXS/ID/ASD, containing factors associated with Ras/mitogen-activated protein kinase, Wnt/β-catenin, and mammalian target of rapamycin (mTOR) pathways. We indeed showed overactivation of mTOR signaling via an increase in mTOR phosphorylation in the Fmr1 knockout (Fmr1 KO) neocortex. Our results provide further insight into the critical roles of FMRP in the developing brain, where dysfunction of FMRP may influence the regulation of its mRNA targets affecting signaling pathways and epigenetic modifications.

Cadmium inhibits neurogenesis in zebrafish embryonic brain development

2008 ◽  
Vol 87 (3) ◽  
pp. 157-169 ◽  
Author(s):  
Elly Suk Hen Chow ◽  
Michelle Nga Yu Hui ◽  
Chun Chi Lin ◽  
Shuk Han Cheng
Keyword(s):  
Brain Development ◽  
Embryonic Brain ◽  
Embryonic Brain Development

scholarly journals Ultrasound backscatter microscope analysis of early mouse embryonic brain development.

1995 ◽  
Vol 92 (6) ◽  
pp. 2239-2243 ◽  
Author(s):  
D. H. Turnbull ◽  
T. S. Bloomfield ◽  
H. S. Baldwin ◽  
F. S. Foster ◽  
A. L. Joyner
Keyword(s):  
Brain Development ◽  
Embryonic Brain ◽  
Microscope Analysis ◽  
Ultrasound Backscatter ◽  
Early Mouse ◽  
Embryonic Brain Development

Involvement of thyroid hormones in chicken embryonic brain development

2009 ◽  
Vol 163 (1-2) ◽  
pp. 58-62 ◽  
Author(s):  
Veerle M. Darras ◽  
Stijn L.J. Van Herck ◽  
Stijn Geysens ◽  
Geert E. Reyns
Keyword(s):  
Thyroid Hormones ◽  
Brain Development ◽  
Embryonic Brain ◽  
Embryonic Brain Development

scholarly journals Large-scale identification of RBP-RNA interactions by RAPseq refines essentials of post-transcriptional gene regulation

2021 ◽  
Author(s):  
Ionut Atanasoai ◽  
Sofia Papavasileiou ◽  
Natalie Preiss ◽  
Claudia Kutter
Keyword(s):  
Binding Sites ◽  
Large Scale ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Affinity Purification ◽  
Binding Motif ◽  
The Past ◽  
Optimal Distance ◽  
Transcriptional Gene Regulation

Over the past decade, thousands of putative human RNA binding proteins (RBPs) have been identified and increased the demand for specifying RNA binding capacities. Here, we developed RNA affinity purification followed by sequencing (RAPseq) that enables in vitro large-scale profiling of RBP binding to native RNAs. First, by employing RAPseq, we found that vertebrate HURs recognize a conserved RNA binding motif and bind predominantly to introns in zebrafish compared to 3'UTRs in human RNAs. Second, our dual RBP assays (co-RAPseq) uncovered cooperative RNA binding of HUR and PTBP1 within an optimal distance of 27 nucleotides. Third, we developed T7-RAPseq to discern m6A-dependent and -independent RNA binding sites of YTHDF1. Fourth, RAPseq of 26 novel non-canonical RBPs revealed specialized moonlighting interactions. Last, five pathological IGF2BP family variants exhibited different RNA binding patterns. Overall, our simple, scalable and versatile method enables to fast-forward RBP-related questions.

The Genetics of Embryonic Brain Development inDrosophila

1998 ◽  
Vol 12 (4-5) ◽  
pp. 194-205 ◽  
Author(s):  
Beate Hartmann ◽  
Heinrich Reichert
Keyword(s):  
Brain Development ◽  
Embryonic Brain ◽  
Embryonic Brain Development
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