Yersinia pestis

Yersinia pestis is a gram-negative, non-motile, rod-shaped, coccobacillus bacterium, with no spores. It is a facultative anaerobic organism, it causes the disease plague, which takes three main forms: pneumonic and bubonic. All three forms have been responsible for high-mortality epidemics throughout human history, including the Plague of Justinian in the sixth century; those plagues originated in China and were transmitted west via trade routes. Research in 2018 indicated that the pathogen may have been the cause of what has been described as the Neolithic decline, in which European populations declined significantly; that would push the date to much earlier, might indicate an origin in Europe rather than Eurasia. Y. pestis was discovered in 1894 by Alexandre Yersin, a Swiss/French physician and bacteriologist from the Pasteur Institute, during an epidemic of the plague in Hong Kong. Yersin was a member of the Pasteur school of thought. Kitasato Shibasaburō, a German-trained Japanese bacteriologist who practised Koch's methodology, was engaged at the time in finding the causative agent of the plague.

However, Yersin linked plague with Y. pestis. Named Pasteurella pestis, the organism was renamed Yersinia pestis in 1944; every year, thousands of cases of the plague are still reported to the World Health Organization, although with proper treatment, the prognosis for victims is now much better. A five- to six-fold increase in cases occurred in Asia during the time of the Vietnam War due to the disruption of ecosystems and closer proximity between people and animals; the plague is now found in sub-Saharan Africa and Madagascar, areas which now account for over 95% of reported cases. The plague has a detrimental effect on nonhuman mammals. In the United States, mammals such as the black-tailed prairie dog and the endangered black-footed ferret are under threat. Y. pestis is a nonmotile, stick-shaped, facultative anaerobic bacterium with bipolar staining that produces an antiphagocytic slime layer. Similar to other Yersinia species, it tests negative for urease, lactose fermentation, indole, its closest relative is the gastrointestinal pathogen Yersinia pseudotuberculosis, more distantly Yersinia enterocolitica.

A complete genomic sequence is available for two of the three subspecies of Y. pestis: strain KIM, strain CO92. As of 2006, the genomic sequence of a strain of biovar Antiqua has been completed. Similar to the other pathogenic strains, signs exist of loss of function mutations; the chromosome of strain KIM is 4,600,755 base pairs long. Like Y. pseudotuberculosis and Y. enterocolitica, Y. pestis is host to the plasmid pCD1. It hosts two other plasmids, pPCP1 and pMT1 that are not carried by the other Yersinia species. PFra codes for a phospholipase D, important for the ability of Y. pestis to be transmitted by fleas. PPla codes for a protease, that activates plasmin in human hosts and is a important virulence factor for pneumonic plague. Together, these plasmids, a pathogenicity island called HPI, encode several proteins that cause the pathogenesis, for which Y. pestis is famous. Among other things, these virulence factors are required for bacterial adhesion and injection of proteins into the host cell, invasion of bacteria in the host cell, acquisition and binding of iron harvested from red blood cells.

Y. pestis is thought to be descended from Y. pseudotuberculosis, differing only in the presence of specific virulence plasmids. A comprehensive and comparative proteomics analysis of Y. pestis strain KIM was performed in 2006. The analysis focused on the transition to a growth condition mimicking growth in host cells. Numerous bacterial small noncoding RNAs have been identified to play regulatory functions; some can regulate the virulence genes. Some 63 novel putative sRNAs were identified through deep sequencing of the Y. pestis sRNA-ome. Among them was Yersinia-specific Ysr141. Ysr141 sRNA was shown to regulate the synthesis of the type III secretion system effector protein YopJ; the Yop-Ysc T3SS is a critical component of virulence for Yersinia species. Many novel sRNAs were identified from Y. pestis grown in vitro and in the infected lungs of mice suggesting they play role in bacterial physiology or pathogenesis. Among them sR035 predicted to pair with SD region and transcription initiation site of a thermo-sensitive regulator ymoA, sR084 predicted to pair with fur, ferric uptake regulator.

In the urban and sylvatic cycles of Y. pestis, most of the spreading occurs between rodents and fleas. In the sylvatic cycle, the rodent is wild, but in the urban cycle, the rodent is the brown rat. In addition, Y. pestis can spread from the urban environment and back. Transmission to humans is through the bite of infected fleas. If the disease has progressed to the pneumonic form, humans can spread the bacterium to others by coughing and sneezing. Several species

Anthony Young, Baron Young of Norwood Green

Anthony Ian Young, Baron Young of Norwood Green is a British politician and Labour Party life peer in the House of Lords. He had been General Secretary of the National Communications Union joint General Secretary Senior Deputy General Secretary of the Communication Workers Union, he served as a Governor of the BBC. In the 2002 Birthday Honours Young was awarded a knighthood, having the honour conferred by The Prince of Wales on 13 December 2002, he was created a life peer on 25 June 2004 taking the title Baron Young of Norwood Green, of Norwood Green in the London Borough of Ealing. In October 2008 he was appointed as Parliamentary Under-Secretary of State for Skills and Apprenticeships in the Department for Innovation and Skills, being moved to the Department for Business and Skills when it was created in the June 2009 reshuffle, continuing as a Parliamentary Under Secretary of State, but with responsibility for Employment Relations and Postal Affairs until 11 May 2010


Transmembrane protein 229b is a protein that in humans is encoded by the TMEM229b gene. The TMEM229B gene is known as C14orf83, FLJ33387, Q8NBD8, Hs.509707, Hs.712258, IPR010540, CN083_HUMAN. The TMEM229B gene is located on the sense strand of chromosome 14 at location 14q24.1 and spans the chromosomal locus 67,936,983—67,982,021. Covering a total of 45,038 base pairs along the chromosome, the TMEM229B gene has a total of 3 exons in its primary unspliced transcript mRNA of 4,068 bp. There are a total of 7 transcript variants for TMEM229B ranging in mRNA size from 519 bp to 5008 bp; the TMEM229B gene is flanked by phosphatidylinotisol glycan anchor class H, a protein associated with the endoplasmic reticulum GPI-anchor biosynthesis, PLEK2 on its left. See Figure 1.0. The gene is conserved in vertebrates, including portions of the 3,000 base pairs of 3'UTR. Expressed sequence tag mapping of TMEM229B gene expression indicates that it is ubiquitously expressed throughout the body. TMEM229B is more expressed in the parathyroid and thyroid tissues, moderately expressed in bone marrow, spleen, brain, mammary gland, liver, lymph node, muscle, lung and kidney tissues.

The translated TMEM229B protein is a total of 167 amino acids long, with a predicted molecular weight of 19,531 Daltons. The TMEM229B protein contains a domain of unknown function, part of the domain family DUF1113, spanning from amino acids 87 to 135. Based on predicted structure TMEM229b is resemblant of a connexin subunit. A conserved phosphorylation site exists at the Threonine-139 position. See multiple sequence alignment below. Expression of the TMEM229B gene increases in several disease states including amelanotic skin melanoma, B-cell neoplasm, breast carcinoma, Burkitt's lymphoma, colorectal adenocarcinoma, cutaneous T cell lymphoma, esophageal carcinoma, gastric carcinoma, liver carcinoma, melanoma, small cell lung carcinoma, T-cell acute lymphoblastic leukemia, thyroid carcinoma and Wilms' tumor as found in several microarray experiments. Over-expression of the TMEM229B gene has not been linked as a causal factor in any of these disease states