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Yeast repair gapped plasmids by homologous recombination

Posted by star on 2018-09-29 19:10:27
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    Additional information about HR was gained by transforming yeast cells with recombinant plasmids that have yeast genes but lack a yeast replicator sequence. Because the plasmids lack a yeast replicator, their yeast genes can only be maintained if they integrate into the yeast genome. Early experiments showed that plasmids integrated into the yeast genome by HR between the yeast gene on the plasmid and the homologous yeast gene in the chromosomal DNA.

    Terry Orr- Weaver, Jack Szostak, and Rodney Rothstein performed experiments with a yeast transforming plasmid that lacks a yeast replicator and is therefore incapable of autonomous replication. The yeast plasmid carried two yeast markers derived from different chromosomal genes. In some experiments, they used a restriction endonuclease to make one double-strand break in one of the two genes and in other experiments they used two restriction endonucleases to make two double-strand breaks in one of the genes, removing an internal sequence and creating a gap. Surprisingly, the broken plasmids transformed at much higher frequencies than the uncut plasmid. Ail of the transformants were the result, of integration of the plasmid into chromosomal DNA. The plasmid was integrated at the homologous gene sequence in the chromosome and, moreover, the gapped plasmid was repaired during the transformation and integration process. These experiments showed that double-strand breaks stimulate HR. This formed the basis for a new HR model.



The Holliday junction

Posted by star on 2018-09-27 19:25:41
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    Robin Holliday proposed a model for HR in meiosis. According to this model, recombination begins after DNA replication. An endonuclease is proposed to introduce a single nick into each duplex so that strands with the same orientation in each duplex are nicked at the same site. Next, symmetric exchange of single DNA strands between duplexes occurs to form what is called symmetric het eroduplex DNA. The crossed strand structure is an important intermediate and is called the Holliday junction. This structure has four-way symmetry and can move down the paired chromatids by a process called branch migration, forming more heteroduplex DNA. At some point, the Holliday Junction structure is cleaved to generate two separate nicked duplexes, a process known as resolution. Because the Holliday junction has four-way symmetry, it can be resolved in an east-west direction, giving noncrossover products, or in a north-south direction, giving crossover products. Mismatch repair of the heteroduplex DNA region can either restore the original genotype or change the genotype of one (e. g., A)to the other (e. g., a). This change gives a 1:3 (or 3:1) segregation and explains the association of gene conversion with crossovers in the flanking region.

    The Holliday model has several shortcomings. As described below, recombination is now known to begin at a double-strand break or single-strand gap in one DNA molecule. Furthermore, even though extensive efforts have been made to detect an endonuclease with the specificity required by the model, no such enzyme has been found in eukaryotes although much progress has been made in identifying biochemical resolution activities. Despite these shortcomings, the Holliday model has made an important contribution to our understanding of DNA recombination and several features of the model, including the heteroduplex DNA intermediate, branch migration, the Holliday junction, and resolution, remain an importa......

RecBCD compounds

Posted by star on 2018-09-27 19:20:26
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    The double-strand break that precedes recombination must be processed before recombination can take place. This processing is performed by the RecBCD protein complex, which cuts back or resects the double-strand break DNA end. RecB and recC mutants were isolated in initial screens for conjugation-defective and UV-sensitive E. coli mutants. Later studies showed that the RecB and Recc proteins act in a complex that also contains the ReeD protein. The RecBCD complex has several biochemical activities a 3'→5'exonuclease activity, a 5'→3'exonuclease activity, and a DNA helicase activity. These three activities work together to prepare the double-strand break end for HR. The RecBCD complex binds to double-strand break ends and then unwinds the double strand through the helicase activity while degrading each single strand separately. Degradation of two single strands occurs at different rates, with the 3'→5'exonuclease activity being predominant, so that the 3' end is degraded more rapidly. This degradation pattern continues until the RecBCD complex reaches a sequence called a chi site.

    Chi sites were discovered by investigators who were studying phage mutants with defects in their recombination system. These recombination-deficient (red) mutants depend on the bacterial RecBCD complex to perform the essential recombination functions needed for viral DNA replication. Because the bacterial recombination system is a poor substitute for the phage system, bacterial infection produces small plaques. However a few large plaques sometimes are formed. Lambda phages isolated from these large plaques were shown to have an additional mutation that created hot spots (now called chi sites), which allowed the bacterial RecBCD complex to function more efficiently.

    Subsequent studies showed that cbi sites have the sequence 5'-GCTGGTGG-3'and are quite common inthe bacterial genome, occurring about onc......

Extreme daytime sleepiness may increase the risk of Alzheimer disease

Posted by star on 2018-09-27 19:08:14
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    Extreme daytime sleepiness (EDS) is common in the elderly. However, a recent study found that extreme daytime sleepiness may be associated with an increased risk of Alzheimer's disease. The report says people who are sleepy during the day are nearly three times more likely to have beta-amyloid deposits in their brains than those who are not sleepy, and beta-amyloid is the hallmark of Alzheimer's disease.

    This study was published in the journal SLEEP under the title "Excessive daytime sleepiness and napping in cognitively normal adults: associations with subsequent amyloid deposition measured by PiB PET".

    The researcher analyzed data from 124 volunteers aged 60 years to see which reports of daytime sleepiness or nap and were associated with beta-amyloid deposition in the brain.

    The results of the study showed that those who reported daytime sleepiness were three times more likely to develop amyloid deposits. After adjusting for factors such as age, gender, education, and body mass index that may affect daytime sleepiness, the risk of daytime sleepiness is still 2.75 times higher.

    Animal model studies of Alzheimer's disease have shown that limiting nighttime sleep results in more beta-amyloid in the brain and spinal fluid. Some human studies have shown that lack of sleep is associated with increased beta-amyloid content in nerve tissue.

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    In a new study, it is reported that in a mouse model of brain disease, senescent cells accumulate in their brains before cognitive loss. By preventing the accumulation of these aging cells, they are able to reduce tau protein accumulation, neuronal death and memory loss. The results of the study were published on September 19, 2018 in the Nature, entitled "Aging glial cells prevent tau-dependent pathology and cognitive decline."

    It is known that senescent cells accumulate in sites associated with aging diseases (including osteoarthritis and atherosclerosis) and neurodegenerative diseases (including Alzheimer and Parkinson) as they age. In previous studies, the researchers have found that removing senescent cells from naturally aged mice prolongs their healthy lifespan.

    The new study used a mouse model that mimicked Alzheimer. They produce sticky, spider-like tau protein tangles in their neurons and after gene was modified, their senescent cells can be cleared.When senescent cells were removed, they found that the diseased mice maintained the ability to form memory and eliminate signs of inflammation, did not produce neurofibrillary tangles, and maintained normal brain quality. They also reported that drug intervention to remove senescent cells can regulate the accumulation of tau protein.

    In addition, the researchers was able to identify specific cell types that are senescent. When the brain tissue was observed under a microscope, they found two different types of brain cells called microglia and astrocytes to age. These cells are important proponents of neuronal health and signaling, so it makes sense that aging of any of these cells can have a negative impact on neuronal health.


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