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Y Emura

Publications and source records attributed to Y Emura.

5 recordsLinked to original sources

The meiotic recombination hot spot created by the single-base substitution ade6-M26 results in remodeling of chromatin structure in fission yeast.

The G -->T transversion mutation, ade6-M26, creates the heptanucleotide sequence ATGACTG, which lies close to the 5' end of the open reading frame of the ade6 gene in Schizosaccharomyces pombe. The mutation generates a meiosis-specific recombination hot spot and a binding site for the Mts1/Mts2 protein. We examined the chromatin structure at the ade6 locus in the M26 strain and compared it to that of the wild-type and hot spot-negative control M375. Micrococcal nuclease (MNase) digestion and indirect end-labeling methods were applied. In the M26 strain, we detected a new MNase-hypersensitive site at the position of the M26 mutation and no longer observed the phasing of nucleosomes seen in the wild-type and the M375 strains. Quantitative comparison of MNase sensitivity of the chromatin in premeiotic and meiotic cultures revealed a small meiotic induction of MNase hypersensitivity in the ade6 promoter region of the wild-type and M375 strains. The meiotic induction of MNase hypersensitivity was enhanced significantly in the ade6 promoter region of the M26 strain and also occurred at the M26 mutation site. The formation of the MNase-sensitive region around the heptamer sequence was abolished by the introduction of single-nucleotide substitutions in the heptamer sequence, which also abolish hot spot activity and binding of Mts1/Mts2. These data suggest that Mts1/Mts2 binding to the heptamer sequence results in a chromatin structure suitable for the recruitment of a meiosis-specific recombination function or functions.

Chromatin↗

Acute left ventricular dysfunction and left ventricular thrombus in a patient with cerebral hemorrhage.

A 66-year-old woman was admitted to the hospital with a cerebral hemorrhage. An echocardiogram showed severe left ventricular hypokinesis and a left ventricular thrombus. An electrocardiogram showed ST segment elevation in the precordial leads. The patient's creatine kinase level was elevated. A follow-up echocardiogram performed 1 month after admission showed normalization of left ventricular wall motion and disappearance of the thrombus. The results of thallium myocardial scintigraphy, coronary arteriography, and left ventriculography performed 1 month after admission were normal, and the patient was discharged without clinical sequelae. The cause of the patient's left ventricular dysfunction was believed to be not myocardial infarction or myocarditis, but a massive adrenergic discharge due to the cerebral hemorrhage.

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