13 research outputs found
Physiological effects of KDM5C on neural crest migration and eye formation during vertebrate development
Background: Lysine-specific histone demethylase 5C (KDM5C) belongs to the jumonji family of demethylases and is specific for the di- and tri-demethylation of lysine 4 residues on histone 3 (H3K4 me2/3). KDM5C is expressed in the brain and skeletal muscles of humans and is associated with various biologically significant processes. KDM5C is known to be associated with X-linked mental retardation and is also involved in the development of cancer. However, the developmental significance of KDM5C has not been explored yet. In the present study, we investigated the physiological roles of KDM5C during Xenopus laevis embryonic development.
Results: Loss-of-function analysis using kdm5c antisense morpholino oligonucleotides indicated that kdm5c knockdown led to small-sized heads, reduced cartilage size, and malformed eyes (i.e., small-sized and deformed eyes). Molecular analyses of KDM5C functional roles using whole-mount in situ hybridization, -galactosidase staining, and reverse transcription-polymerase chain reaction revealed that loss of kdm5c resulted in reduced expression levels of neural crest specifiers and genes involved in eye development. Furthermore, transcriptome analysis indicated the significance of KDM5C in morphogenesis and organogenesis.
Conclusion: Our findings indicated that KDM5C is associated with embryonic development and provided additional information regarding the complex and dynamic gene network that regulates neural crest formation and eye development. This study emphasizes the functional significance of KDM5C in Xenopus embryogenesis; however, further analysis is needed to explore the interactions of KDM5C with specific developmental genes
Lawson criterion for ignition exceeded in an inertial fusion experiment
For more than half a century, researchers around the world have been engaged in attempts to achieve fusion ignition as a proof of principle of various fusion concepts. Following the Lawson criterion, an ignited plasma is one where the fusion heating power is high enough to overcome all the physical processes that cool the fusion plasma, creating a positive thermodynamic feedback loop with rapidly increasing temperature. In inertially confined fusion, ignition is a state where the fusion plasma can begin "burn propagation" into surrounding cold fuel, enabling the possibility of high energy gain. While "scientific breakeven" (i.e., unity target gain) has not yet been achieved (here target gain is 0.72, 1.37 MJ of fusion for 1.92 MJ of laser energy), this Letter reports the first controlled fusion experiment, using laser indirect drive, on the National Ignition Facility to produce capsule gain (here 5.8) and reach ignition by nine different formulations of the Lawson criterion
Inflammatory response after open and laparoscopic Nissen fundoplication in children: a randomized study
Selenium-Based S-Adenosylmethionine Analog Reveals the Mammalian Seven-Beta-Strand Methyltransferase METTL10 to Be an EF1A1 Lysine Methyltransferase
One crisis, diverse impacts—Tissue-specificity of folate deficiency-induced circulation defects in zebrafish larvae
Neural crest specification and migration independently require NSD3-related lysine methyltransferase activity
Genetics of vesicoureteral reflux
Primary vesicoureteral reflux (VUR) is the most common urological anomaly in children, affecting
1–2% of the pediatric population and 30–40% of children presenting with urinary tract infections (UTIs). Refluxassociated
nephropathy is a major cause of childhood hypertension and chronic renal failure. The hereditary
and familial nature of VUR is well recognized and several studies have reported that siblings of children
with VUR have a higher incidence of reflux than the general pediatric population. Familial clustering of VUR
implies that genetic factors have an important role in its pathogenesis, but no single major locus or gene for
VUR has yet been identified and most researchers now acknowledge that VUR is genetically heterogeneous.
Improvements in genome-scan techniques and continuously increasing knowledge of the genetic basis of VUR
should help us to further understand its pathogenesis.Other funderChildren's Medical and Research Foundation6M embargo after publication - AV 8/9/2011
ke, SB-09/09/201