Open AccessDistribution of chromosome breaks in measles, Fanconi's anemia and controls
Author(s) -
KOSKULL HARRIET,
AULA PERTTI
Publication year - 1977
Publication title -
hereditas
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.819
H-Index - 50
eISSN - 1601-5223
pISSN - 0018-0661
DOI - 10.1111/j.1601-5223.1977.tb01238.x
Subject(s) - biology , chromatid , chromosome , fanconi anemia , genetics , measles , microbiology and biotechnology , virology , dna , dna repair , gene , vaccination
The localization of breaks in human chromosomes was analyzed in three materials: Acute measles, Fanconi's anemia and controls (cases karyotyped because of a suspected chromosome anomaly). The breaks were localized in G‐banded chromosome preparations from lymphocyte cultures. The number of breaks observed in a chromosome region was compared to the number of breaks expected on the basis of the relative length of the region. There were 382 breaks in six measles patients, 423 breaks in five cases of Fanconi's anemia and 369 breaks in 264 control cases. The chromosome and chromatid breaks, found in the whole material, were located, with three exceptions, in the lighly stained G‐bands. The distribution of breaks in the chromosome regions was non‐random in all three groups of cultures. The non‐randomness displayed a similar pattern in the measles as in the controls, but was distinctly different in Fanconi's anemia. The middle region of the short arm of chromosome 3 (3p2) displayed the heaviest clustering of breaks in measles and control patients (12% and 13%, respectively, of all breaks). Regions 9q1 and 16q2 also showed a clustering of breaks both in measles and in controls. In Fanconi's anemia other regions, 3q2 and 13q3 particularly, had more breaks than expected. The results suggest that analysis of the localization of chromosome breaks might give information on the cause and mechanism of chromosome breakage.