scholarly journals Expression patterns of TRα and CRABPII genes in Chinese cashmere goat skin during prenatal development

2015 ◽  
Vol 57 (1) ◽  
Author(s):  
Tao Zhong ◽  
Wei Zhao ◽  
Zhongqiang Zhou ◽  
Li Li ◽  
Linjie Wang ◽  
...  
2021 ◽  
Vol 15 ◽  
Author(s):  
Chao Fang ◽  
Hong Wang ◽  
Robert Konrad Naumann

The claustrum is an enigmatic brain structure thought to be important for conscious sensations. Recent studies have focused on gene expression patterns, connectivity, and function of the claustrum, but relatively little is known about its development. Interestingly, claustrum-enriched genes, including the previously identified marker Nurr1, are not only expressed in the classical claustrum complex, but also embedded within lateral neocortical regions in rodents. Recent studies suggest that Nurr1 positive neurons in the lateral cortex share a highly conserved genetic expression pattern with claustrum neurons. Thus, we focus on the developmental progression and birth dating pattern of the claustrum and Nurr1 positive neurons in the lateral cortex. We comprehensively investigate the expression of Nurr1 at various stages of development in the rat and find that Nurr1 expression first appears as an elongated line along the anterior-posterior axis on embryonic day 13.5 (E13.5) and then gradually differentiates into multiple sub-regions during prenatal development. Previous birth dating studies of the claustrum have led to conflicting results, therefore, we combine 5-ethynyl-2′-deoxyuridine (EdU) labeling with in situ hybridization for Nurr1 to study birth dating patterns. We find that most dorsal endopiriform (DEn) neurons are born on E13.5 to E14.5. Ventral claustrum (vCL) and dorsal claustrum (dCL) are mainly born on E14.5 to E15.5. Nurr1 positive cortical deep layer neurons (dLn) and superficial layer neurons (sLn) are mainly born on E14.5 to E15.5 and E15.5 to E17.5, respectively. Finally, we identify ventral to dorsal and posterior to anterior neurogenetic gradients within vCL and DEn. Thus, our findings suggest that claustrum and Nurr1 positive neurons in the lateral cortex are born sequentially over several days of embryonic development and contribute toward charting the complex developmental pattern of the claustrum in rodents.


2000 ◽  
Vol 278 (5) ◽  
pp. R1305-R1313 ◽  
Author(s):  
Yvonne H. J. M. Arens ◽  
Charles R. Rosenfeld ◽  
Kristine E. Kamm

Maturation rates of vascular and visceral smooth muscle (SM) during ovine development were compared by quantifying contractile protein, myosin heavy chain (MHC) isoform contents, and contractile properties of aortas and bladders from female fetal ( n = 19) and postnatal ( n = 21) sheep. Actin, myosin, and protein contents rose progressively throughout development in both tissues ( P ≤ 0.003); however, expression patterns differed. During the last trimester, i.e., 101–130 days (term ∼145 days), bladder actin and MHC contents were approximately twofold greater ( P < 0.04) than those in the aorta. Although the fractional content of 204-kDa SM1 MHC in the bladder decreased from 74 ± 3% at midgestation to 48 ± 2% 3 mo postnatal, the aorta exhibited an increase from 30 ± 2% to 65 ± 2%. Bladder MHC (MHC-B) migrating at 200 kDa contained only SM2 throughout development. In contrast, 200-kDa MHC in the aorta was predominantly nonmuscle MHC-B at midgestation, which was gradually replaced by SM2 as development progressed. Along with its early expression of SM2, bladder muscle obtained maximal stress generating capacity (1.7 × 105 N/m2) by term gestation, whereas the aorta exhibited no contractions until after birth. We conclude that whereas aortic SM maturation is delayed until after birth, bladder SM matures biochemically and functionally during prenatal development, thus supporting early requirements for micturition.


2018 ◽  
Author(s):  
Sorena Rahmanian ◽  
Rabi Murad ◽  
Alessandra Breschi ◽  
Weihua Zeng ◽  
Mark Mackiewicz ◽  
...  

ABSTRACTMicroRNAs (miRNAs) play a critical role as post-transcriptional regulators of gene expression. The ENCODE project profiled the expression of miRNAs in a comprehensive set of tissues during a time-course of mouse embryonic development and captured the expression dynamics of 785 miRNAs. We found distinct tissue and developmental stage specific miRNA expression clusters, with an overall pattern of increasing tissue specific expression as development proceeds. Comparative analysis of conserved miRNAs in mouse and human revealed stronger clustering of expression patterns by tissue types rather than by species. An analysis of messenger RNA gene expression clusters compared with miRNA expression clusters identifies the potential role of specific miRNA expression clusters in suppressing the expression of mRNAs specific to other developmental programs in the tissue where these microRNAs are expressed during embryonic development. Our results provide the most comprehensive timecourse of miRNA expression as an integrated part of the ENCODE reference dataset for mouse embryonic development.


PLoS ONE ◽  
2012 ◽  
Vol 7 (12) ◽  
pp. e50001 ◽  
Author(s):  
Zhihong Liu ◽  
Hongmei Xiao ◽  
Huipeng Li ◽  
Yanhong Zhao ◽  
Shuangying Lai ◽  
...  

2014 ◽  
Vol 42 (5) ◽  
pp. 989-995 ◽  
Author(s):  
Rui Su ◽  
Shaoyin Fu ◽  
Yanjun Zhang ◽  
Ruijun Wang ◽  
Yanhong Zhou ◽  
...  

1996 ◽  
Vol 45 (1-2) ◽  
pp. 91-92
Author(s):  
R. Ohlsson ◽  
T.J. Ekström ◽  
G. Adam ◽  
S. Miller ◽  
H. Cui ◽  
...  

Genetic imprinting implies the preferential or exclusive expression of one of the parental alleles of a subset of autosomal loci. The insulin-like growth factor II (IGF2) and H19 loci are particularly interesting examples of this phenomenon since their products appear to display growth agonistic and antagonistic properties, respectively. In addition, IGF2 and H19 are only 90 kb apart, are expressed from opposite parental alleles [1,2] and show a striking similarity in their spatial expression patterns during human prenatal development [3]. One exception is the choroid plexus and leptomeninges which express 1GF2 biallically with no detectable H19 expression [3]. Observations like these have fuelled ideas that there is an enhancer competition between the IGF2 and H19 loci [4]. The imprinting status of the H19 locus would then indirectly control the expressivity of IGF2. This model is likely to be too simple since the P1 promoter of IGF2 is not functionally imprinted during liver development in humans [4]. Moreover, while the liver P2-P4 promoters are expressed primarily from the paternally derived allele during human prenatal development, the P2-P4 promoters can be expressed from both parental alleles in complex patterns during postnatal human development [5]. The enhancer competition model might be put to the test in human and mouse uniparental embryos since the parental origin of their diploid genomes cannot be discerned. Unexpectedly, H19 which is expressed preferentially from the maternal allele in mouse [6] and human [7] placenta is expressed in both mouse and human trophoblasts (in complete hydatidiform moles) lacking the maternal genome. In the normal human placenta, the repressed paternal H19 allele is more methylated. Interestingly, the CpG methylation pattern of H19 is strikingly similar between normal placenta and complete moles. Hence, both paternal H19 alleles are similarly methylated indicating that postzygotic modification events typical of normal development have taken place in complete moles as well in spite of the absence of the maternal genome. In contrast to the normal placenta, H19 is expressed biallelically in complete moles as assessed by allele-specific in situ hybridisation analysis of dispermie moles [8]. We discuss these results in relation to current models of IGF2/H19 imprinting mechanism(s).


2009 ◽  
Vol 8 (4) ◽  
pp. 491-496 ◽  
Author(s):  
Jiang-hong WU ◽  
Wen-guang ZHANG ◽  
Jin-quan LI ◽  
Jun YIN ◽  
Yan-jun ZHANG

2021 ◽  
Author(s):  
Egidio Spinelli ◽  
Kyle R Christensen ◽  
Emily Bryant ◽  
Amy Schneider ◽  
Jennifer Rakotomamonjy ◽  
...  

AbstractObjectiveThe MAST family of microtubule-associated serine-threonine kinases (STK) have distinct expression patterns in the developing and mature human and mouse brain. To date, only MAST1 has been associated with neurological disease, with de novo variants in individuals with a neurodevelopmental disorder, including a mega corpus callosum.MethodsUsing exome sequencing we identify MAST3 missense variants in individuals with epilepsy. We also assess the effect of these variants on the ability of MAST3 to phosphorylate the target gene product ARPP-16 in HEK293T cells.ResultsWe identify de novo missense variants in the STK domain in 11 individuals, including two recurrent variants p.G510S (n=5) and p.G515S (n=3). All 11 individuals had Developmental and epileptic encephalopathy, with 8 having normal development prior to seizure onset at < 2 years of age. All patients developed multiple seizures types, while 9/11 had seizures triggered by fever and 9/11 had drug-resistant seizures. In vitro analysis of HEK293T cells transfected with MAST3 cDNA carrying a subset of these patient-specific missense variants demonstrated variable but generally lower expression, with concomitant increased phosphorylation of the MAST3 target, ARPP-16, compared to wildtype. These findings suggest the patient-specific variants may confer MAST3 gain-of-function. Moreover, single-nuclei RNA sequencing and immunohistochemistry shows that MAST3 expression is restricted to excitatory neurons in the cortex late in prenatal development and postnatally.InterpretationIn summary, we describe MAST3 as a novel epilepsy-associated gene with a potential gain-of-function pathogenic mechanism that may be primarily restricted to excitatory neurons in the cortex.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Yuanyuan Zheng ◽  
Taiyu Hui ◽  
Chang Yue ◽  
Jiaming Sun ◽  
Dan Guo ◽  
...  

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