scholarly journals Spatial patterns of gene expression in the olfactory bulb

2004 ◽  
Vol 101 (34) ◽  
pp. 12718-12723 ◽  
Author(s):  
D. M. Lin ◽  
Y. H. Yang ◽  
J. A. Scolnick ◽  
L. J. Brunet ◽  
H. Marsh ◽  
...  
Nutrients ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3909
Author(s):  
Melissa S. Totten ◽  
Derek M. Pierce ◽  
Keith M. Erikson

The aim of this study was to determine the impact of diet-induced obesity (DIO) on trace element homeostasis and gene expression in the olfactory bulb and to identify potential interaction effects between diet, sex, and strain. Our study is based on evidence that obesity and olfactory bulb impairments are linked to neurodegenerative processes. Briefly, C57BL/6J (B6J) and DBA/2J (D2J) male and female mice were fed either a low-fat diet or a high-fat diet for 16 weeks. Brain tissue was then evaluated for iron, manganese, copper, and zinc concentrations and mRNA gene expression. There was a statistically significant diet-by-sex interaction for iron and a three-way interaction between diet, sex, and strain for zinc in the olfactory bulb. Obese male B6J mice had a striking 75% increase in iron and a 50% increase in manganese compared with the control. There was an increase in zinc due to DIO in B6J males and D2J females, but a decrease in zinc in B6J females and D2J males. Obese male D2J mice had significantly upregulated mRNA gene expression for divalent metal transporter 1, alpha-synuclein, amyloid precursor protein, dopamine receptor D2, and tyrosine hydroxylase. B6J females with DIO had significantly upregulated brain-derived neurotrophic factor expression. Our results demonstrate that DIO has the potential to disrupt trace element homeostasis and mRNA gene expression in the olfactory bulb, with effects that depend on sex and genetics. We found that DIO led to alterations in iron and manganese predominantly in male B6J mice, and gene expression dysregulation mainly in male D2J mice. These results have important implications for health outcomes related to obesity with possible connections to neurodegenerative disease.


2019 ◽  
Author(s):  
Jakob Seidlitz ◽  
Ajay Nadig ◽  
Siyuan Liu ◽  
Richard A.I. Bethlehem ◽  
Petra E. Vértes ◽  
...  

AbstractNeurodevelopmental disorders are highly heritable and associated with spatially-selective disruptions of brain anatomy. The logic that translates genetic risks into spatially patterned brain vulnerabilities remains unclear but is a fundamental question in disease pathogenesis. Here, we approach this question by integrating (i) in vivo neuroimaging data from patient subgroups with known causal genomic copy number variations (CNVs), and (ii) bulk and single-cell gene expression data from healthy cortex. First, for each of six different CNV disorders, we show that spatial patterns of cortical anatomy change in youth are correlated with spatial patterns of expression for CNV region genes in bulk cortical tissue from typically-developing adults. Next, by transforming normative bulk-tissue cortical expression data into cell-type expression maps, we further link each disorder’s anatomical change map to specific cell classes and specific CNV-region genes that these cells express. Finally, we establish convergent validity of this “transcriptional vulnerability model” by inter-relating patient neuroimaging data with measures of altered gene expression in both brain and blood-derived patient tissue. Our work clarifies general biological principles that govern the mapping of genetic risks onto regional brain disruption in neurodevelopmental disorders. We present new methods that can harness these principles to screen for potential cellular and molecular determinants of disease from readily available patient neuroimaging data.


1995 ◽  
Vol 269 (4) ◽  
pp. G500-G511 ◽  
Author(s):  
E. D. Gutierrez ◽  
K. J. Grapperhaus ◽  
D. C. Rubin

Despite rapid proliferation, the mammalian intestinal epithelium maintains precise spatial differentiation from crypt to villus tip and from duodenum to colon. During perinatal life, the rodent gut undergoes a dramatic morphogenesis, resulting in formation of the crypt-villus and duodenal-colonic axes. The ontogeny of regional differences in gene expression in the emerging vertical axis has not been well described. We used the liver fatty acid binding protein (L-FABP) and apolipoprotein (apo) AIV genes as markers of neonatal enterocytic differentiation. In situ hybridization analyses revealed that both genes exhibit unique spatial patterns of expression along the jejunal crypt-villus axis during ontogeny, characterized by increased cellular mRNA levels in villus base enterocytes. To examine the requirement for a normal luminal environment to generate these precise patterns of cellular gene expression, we employed intestinal isograft techniques. Fetal intestines were implanted as early as embryonic day 12. Appropriate expression of the apo AIV and L-FABP genes was recapitulated during villus morphogenesis in fetal life. However, spatial patterns of gene expression in the isografted postnatal cryptvillus axis were altered. The preferential accumulation of L-FABP and apo AIV mRNA in villus base enterocytes was never observed in isografts. These results suggest that a “basal” differentiation program is encoded in fetal endoderm and mesenchyme, yet extracellular substances contained in the lumen or extrinsic to the intestine play an important modulatory role in generating spatial differentiation during ontogeny.


Cell ◽  
1986 ◽  
Vol 47 (2) ◽  
pp. 285-296 ◽  
Author(s):  
Enrico S. Coen ◽  
Rosemary Carpenter ◽  
Cathie Martin

1990 ◽  
Vol 32 (1) ◽  
pp. 9-13 ◽  
Author(s):  
Koji Akasaka ◽  
Takayuki Ueda ◽  
Toru Higashinakagawa ◽  
Kazumi Yamada ◽  
Hiraku Shimada

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