Bacteria (singular: bacterium) are a major group of living organisms. The term "bacteria" has variously applied to all prokaryotes or to a major group of them, otherwise called the eubacteria, depending on ideas about their relationships. Here, bacteria is used specifically to refer to the eubacteria. Another major group of bacteria (used in the broadest, non-taxonomic sense) are the Archaea. The study of bacteria is known as bacteriology, a subfield of microbiology.

Bacteria are the most abundant of all organisms. They are ubiquitous in soil, water, and as symbionts of other organisms. Many pathogens are bacteria. Most are minute, usually only 0.5-5.0 μm in their longest dimension, although giant bacteria like Thiomargarita namibiensis and Epulopiscium fishelsoni may grow past 0.5 mm in size. They generally have cell walls, like plant and fungal cells, but bacterial cell walls are normally made out of peptidoglycan instead of cellulose (as in plants) or chitin (as in fungi), and are not homologous with eukaryotic cell walls. Many move around using flagella, which are different in structure from the flagella of other groups.

History

---

The first bacteria were observed by Anton van Leeuwenhoek in 1674 using a single-lens microscope of his own design. The name bacterium was introduced much later, by Ehrenberg in 1828, derived from the Greek word βακτηριον meaning "small stick". Because of the difficulty in describing individual bacteria and the importance of their discovery to fields such as medicine, biochemistry, and geochemistry, the history of bacteriology is generally described as the history of microbiology.

More on [ Bacteria ]

Human Molecular Genetics - current issue

Variation in crossover interference levels on individual chromosomes from human males
Lian, J., Yin, Y., Oliver-Bonet, M., Liehr, T., Ko, E., Turek, P., Sun, F., Martin, R. H. Wed, 13 Aug 2008 00:00:00 -0000
Crossovers (COs) generated by homologous recombination ensure the proper segregation of chromosomes during meiosis. COs exhibit interference, which leads to widely spaced COs along chromosomes. Strong positive CO interference has been found in humans. However, little is known about the extent of human CO interference. In this study, variations in CO interference over the entire human genome and among individuals were analyzed by immunofluorescence combined with fluorescence in situ hybridization of testicular biopsies from 10 control men. These methods allow for direct identification of the frequency and location of COs in specific chromosomes of pachytene cells. The strength of CO interference was estimated by fitting the frequency distribution of inter-CO distances to the gamma model. Positive interference among CO on chromosomes was observed in these men, and the strength of inter-arm interference was significantly stronger than that for intra-arm CO. In addition, interference was observed to act across the centromere. Significant inter-individual and inter-chromosomal variations in the levels of interference were found, with smaller chromosomes exhibiting stronger interference. Discontinuous chromosome regions (gaps) and unsynapsed chromosome regions (splits) in chromosome 9 had both cis and trans effects on CO interference levels. This is the first report that the interference level varies significantly across the whole genome and that, at least in the human male, anomalies in chromosome synapsis play an important role in altering CO interference levels.
Sex differences in a transgenic rat model of Huntington's disease: decreased 17{beta}-estradiol levels correlate with reduced numbers of DARPP32+ neurons in males
Bode, F. J., Stephan, M., Suhling, H., Pabst, R., Straub, R. H., Raber, K. A., Bonin, M., Nguyen, H. P., Riess, O., Bauer, A., Sjoberg, C., Petersen, A., von Horsten, S. Wed, 13 Aug 2008 00:00:00 -0000
Recent clinical studies have highlighted that female sex hormones represent potential neuroprotective mediators against damage caused by acute and chronic brain diseases. This evidence has been confirmed by experimental studies documenting the protective role of female sex hormones both in vitro and in vivo, although these studies did not specifically focus on Huntington's disease (HD). We therefore investigated the onset and course of HD in female and male transgenic (tg) HD (CAGn51) and control rats across age and focused on three aspects: (i) behavioral and physiological alterations (energy expenditure, home-cage activity, emotional disturbance and motor dysfunction), (ii) morphological markers (numbers and characteristics of striatal DARPP32+ medium-sized spiny neurons (MSNs) and dopamine receptor autoradiography) and (iii) peripheral sex hormone levels as well as striatal estrogen receptor expression. Independent of their sex, tgHD rats exhibited increased levels of food intake, elevated home-cage activity scores and anxiolytic-like behavior, whereas only males showed an impairment of motor function. In line with the latter finding, loss and atrophy of DARPP32+ MSNs were apparent only in male tgHD rats. This result was associated with a decreased striatal dopamine D1 receptor density and lower plasma levels of 17β-estradiol at the age of 14 months. As DARPP32+ MSNs expressed both - and β-estrogen receptors and showed a correlation between cell numbers and 17β-estradiol levels, our findings suggest sex-related differences in the HD phenotype pointing to a substantial neuroprotective effect of sex hormones and opening new perspectives on the therapy of HD.
Multistep, sequential control of the trafficking and function of the multiple sulfatase deficiency gene product, SUMF1 by PDI, ERGIC-53 and ERp44
Fraldi, A., Zito, E., Annunziata, F., Lombardi, A., Cozzolino, M., Monti, M., Spampanato, C., Ballabio, A., Pucci, P., Sitia, R., Cosma, M. P. Wed, 13 Aug 2008 00:00:00 -0000
Sulfatase modifying factor 1 (SUMF1) encodes for the formylglicine generating enzyme, which activates sulfatases by modifying a key cysteine residue within their catalytic domains. SUMF1 is mutated in patients affected by multiple sulfatase deficiency, a rare recessive disorder in which all sulfatase activities are impaired. Despite the absence of canonical retention/retrieval signals, SUMF1 is largely retained in the endoplasmic reticulum (ER), where it exerts its enzymatic activity on nascent sulfatases. Part of SUMF1 is secreted and paracrinally taken up by distant cells. Here we show that SUMF1 interacts with protein disulfide isomerase (PDI) and ERp44, two thioredoxin family members residing in the early secretory pathway, and with ERGIC-53, a lectin that shuttles between the ER and the Golgi. Functional assays reveal that these interactions are crucial for controlling SUMF1 traffic and function. PDI couples SUMF1 retention and activation in the ER. ERGIC-53 and ERp44 act downstream, favoring SUMF1 export from and retrieval to the ER, respectively. Silencing ERGIC-53 causes proteasomal degradation of SUMF1, while down-regulating ERp44 promotes its secretion. When over-expressed, each of three interactors favors intracellular accumulation. Our results reveal a multistep control of SUMF1 trafficking, with sequential interactions dynamically determining ER localization, activity and secretion.

Subscribe to Genetics RSS feed