scholarly journals Gene Expression Profiling of Listeria monocytogenes Strain F2365 during Growth in Ultrahigh-Temperature-Processed Skim Milk

2008 ◽  
Vol 74 (22) ◽  
pp. 6859-6866 ◽  
Author(s):  
Yanhong Liu ◽  
Amy Ream

ABSTRACT To study how Listeria monocytogenes survives and grows in ultrahigh-temperature-processed (UHT) skim milk, microarray technology was used to monitor the gene expression profiles of strain F2365 in UHT skim milk. Total RNA was isolated from strain F2365 in UHT skim milk after 24 h of growth at 4°C, labeled with fluorescent dyes, and hybridized to “custom-made” commercial oligonucleotide (35-mers) microarray chips containing the whole genome of L. monocytogenes strain F2365. Compared to L. monocytogenes grown in brain heart infusion (BHI) broth for 24 h at 4°C, 26 genes were upregulated (more-than-twofold increase) in UHT skim milk, whereas 14 genes were downregulated (less-than-twofold decrease). The upregulated genes included genes encoding transport and binding proteins, transcriptional regulators, proteins in amino acid biosynthesis and energy metabolism, protein synthesis, cell division, and hypothetical proteins. The downregulated genes included genes that encode transport and binding proteins, protein synthesis, cellular processes, cell envelope, energy metabolism, a transcriptional regulator, and an unknown protein. The gene expression changes determined by microarray assays were confirmed by real-time reverse transcriptase PCR analyses. Furthermore, cells grown in UHT skim milk displayed the same sensitivity to hydrogen peroxide as cells grown in BHI, demonstrating that the elevated levels of expression of genes encoding manganese transporter complexes in UHT skim milk did not result in changes in the oxidative stress sensitivity. To our knowledge, this report represents a novel study of global transcriptional gene expression profiling of L. monocytogenes in a liquid food.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3741-3741
Author(s):  
Sarah M. Mense ◽  
Mei Zhou ◽  
Amitabha Sengupta ◽  
Changgui Lan ◽  
Galina Bentsman ◽  
...  

Abstract Oxygen is vital for the development and survival of mammals. Lack of oxygen and oxygen sensing mechanisms have been implicated in the pathology of many CNS disorders, including stroke, head trauma, neural developmental problems associated with preterm birth, neoplasia and neurodegenerative diseases. In response to hypoxia, the brain initiates numerous adaptive responses at the organ level as well as at the molecular and cellular level, including the alteration of gene expression. Astrocytes play critical roles in the proper functioning of the brain. They are important for maintaining ion and pH homeostasis, for the synthesis and removal of neurotransmitters, such as GABA and glutamate, and for providing glucose supply to the brain. Recent evidence indicates that astrocytes regulate synaptic activity, synaptogenesis, and neurogenesis. Thus, the manner in which astrocytes respond to hypoxia is likely important in determining the outcome of brain hypoxia. Astrocytes are generally more resistant to energy failure than neurons. Astrocytes account for at least 15% of oxidative metabolism in the brain, and their respiratory rates are maintained at 85% of the basal level until oxygen is virtually exhausted. In this report, to better understand the molecular mechanisms governing astrocytic response to hypoxia, we used microarray gene expression profiling and data analysis algorithms to identify and analyze hypoxia-responsive genes in primary human astrocytes. We also compared the gene expression patterns in astrocytes with those of human HeLa cells and pulmonary artery endothelial cells (ECs). Remarkably, in astrocytes, 5 times as many genes were up-regulated as down-regulated, whereas in HeLa and pulmonary ECs, as many or more genes were down-regulated as up-regulated. More genes encoding hypoxia-inducible functions, such as glycolytic enzymes and angiogenic growth factors, were strongly induced in astrocytes compared to HeLa cells. The extent of induction was also greater than in HeLa cells. Further, gene ontology and computational algorithms revealed that many target genes of the EGF and insulin signaling pathways and the transcriptional regulators Myc, Jun and p53 were selectively altered by hypoxia in astrocytes and in HeLa cells to a lesser degree. Figure Figure Figure Figure In the case of astrocytes, the overwhelming induction of target genes of the EGF and insulin pathways, which are pro-survival, and other genes encoding growth factors and functions involved in carbohydrate metabolism may underlie their relative strong resistance to ischemic/hypoxic insults. These results provide a global view of the signaling and regulatory network mediating oxygen regulation in astrocytes, in comparison with that in HeLa cells.


Genomics ◽  
2005 ◽  
Vol 86 (6) ◽  
pp. 657-667 ◽  
Author(s):  
Hanna H. Ng ◽  
Christopher E. Frantz ◽  
Linda Rausch ◽  
David C. Fairchild ◽  
Julie Shimon ◽  
...  

2002 ◽  
Vol 69 ◽  
pp. 135-142 ◽  
Author(s):  
Elena M. Comelli ◽  
Margarida Amado ◽  
Steven R. Head ◽  
James C. Paulson

The development of microarray technology offers the unprecedented possibility of studying the expression of thousands of genes in one experiment. Its exploitation in the glycobiology field will eventually allow the parallel investigation of the expression of many glycosyltransferases, which will ultimately lead to an understanding of the regulation of glycoconjugate synthesis. While numerous gene arrays are available on the market, e.g. the Affymetrix GeneChip® arrays, glycosyltransferases are not adequately represented, which makes comprehensive surveys of their gene expression difficult. This chapter describes the main issues related to the establishment of a custom glycogenes array.


2007 ◽  
Vol 177 (4S) ◽  
pp. 93-93
Author(s):  
Toshiyuki Tsunoda ◽  
Junichi Inocuchi ◽  
Darren Tyson ◽  
Seiji Naito ◽  
David K. Ornstein

2004 ◽  
Vol 171 (4S) ◽  
pp. 198-199 ◽  
Author(s):  
Ximing J. Yang ◽  
Jun Sugimura ◽  
Maria S. Tretiakova ◽  
Bin T. Teh

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