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The control of chiasma distribution.

The question of recombination control has been the subject of intensive investigation over many years. This paper is restricted to an evaluation of the information obtainable from cytological studies of chiasmata, since other approaches are well represented in other papers in this volume. The advantages and disadvantages of chiasmata as means of studying recombination are discussed. Cytological observations reveal many constraints on the distribution of chiasmata, which are interpreted as outward expressions of controls operating at different levels, namely between cells, between bivalents and within bivalents. Detailed descriptions of these constraints are presented as a preliminary to discussing models and mechanisms of control. They include, at the between-bivalent level, over-dispersal of chiasma number per bivalent and the formation of an obligatory minimum of one chiasma per bivalent; and at the within-bivalent level, chiasma localization and chiasma interference. The genetical basis of these constraints is emphasized and evidence presented which suggests that chiasma distribution at different levels is subject to both separate and coordinate genetical controls. These observations lead to the consideration and evaluation of general stochastic models of chiasma control based on the modification of site probabilities for chiasma formation. While these models are a useful approach to thinking about the control of recombination, they do not give a fully satisfactory explanation of all aspects of chiasma control. Finally, specific mechanisms for chiasma distribution control are considered. In a few exceptional species, localized pairing and synaptonemal complexes lead to localized chiasma formation; details of two such cases are presented. In the majority of species, pairing is not localized or restricted and in these species the control of chiasma distribution is more conjectural. Arguments are presented which suggest that even in these cases of full pairing, the pattern of pairing initiation and progression and perhaps the timing of these events could be important factors controlling the distribution of chiasmata.

Animals↗

AML-1 gene rearrangement and AML-1-ETO gene expression as molecular markers of acute myeloblastic leukemia with t(8;21).

Rearrangements of the AML-1 gene on chromosome 21 as well as transcriptional expression of AML-1-ETO fusion gene were studied in 35 leukemic patients with t(8;21)(q22;q22). A panel of probes generated from the AML-1 gene regions flanking the breakpoint on chromosome 21 allowed us to detect the rearrangement in 24 out of 29 patients. A specific nested reverse transcriptase/polymerase chain reaction (RT/PCR) was developed to detect the t(8;21), either at diagnosis or as minimal residual disease. PCR amplification products were obtained in ten out of 11 patients investigated, and the sensitivity of the reaction was estimated to be between 1 x 10(4) and 1 x 10(-5) cell. An AML-1 rearrangement was also detected in one patient with 8q- and only one chromosome 21, but without 21q+. This indicated that the molecular rearrangement of the der(8) chromosome is more important than the reciprocal one in the malignant process.

Adolescent↗

[Lymphomatoid papulosis].

Lymphomatoid papulosis is a distinct entity in which recurring crops of haemorragic and necrotic papules display a cytologically malignant infiltrate. The aberrent cell is now generally accepted to be an active T helper phenotype. The expression of Ki-1 (CD30) on a significant portion of the infiltrating cells characterizes lymphomatoid papulosis and relates this disorder with Hodgkin's disease, mycosis fungoides and anaplasic T cell lymphoma which may be associated in 10 to 20% of lymphomatoid papulosis. The categorization of this disease as a benign disorder versus lymphoma remains controversial. Studies of T cell receptor gene rearrangement demonstrate clonality in many cases. So, this monoclonal population could have a malignant transformation induced by a triggering stimulus such as genetic translocation, or viral infection. Finally, recent opinions consider that lymphomatoid papulosis and Ki-1 (CD30) lymphomas are different parts of a clinical and histological spectrum constituted by cutaneous Ki-1 lymphoid infiltrates.

Antigens, CD↗

[Frequency of radiation-induced exchanges in simian marker chromosomes].

The symmetric and asymmetric exchange frequencies of marked (nucleolus forming) chromosomes were studied in the lymphocytes and epithelial kidney cells irradiated by X-rays at Go, both in vivo and in vitro. Symmetric and asymmetric exchange frequencies were found to be equal. In both the types of Macaca mulatta cells, the exchange frequency in the long arm appeared to be higher than theoretically expected. The increased exchange in the long arm is thought to be due to a greater quantity of late replicating heterochromatin in it. The short arm of marked chromosome of epithelial kidney cells enters the exchange in accordance to its length in mitosis, but exchange number in the short arm chromosome in lymphocytes is lower than in epithelial cells. This difference is caused by different functioning of the nucleolus forming heterochromatin.

Animals↗