Abelson leukemia virus induces lymphoid and erythroid colonies in infected fetal cell cultures.

Abstract:

:An examination of Abelson murine leukemia virus (A-MuL V)-hematopoietic cell interaction in cultures of fetal tissues reveals that A-MuLV can stimulate the formation of two different types of colonies. One type of colony is white and composed of A-MuLV-transformed lymphoid cells that can develop into established cell lines. These cells are indistinguishable in morphology from typical adult-derived lymphoid transformants. The second type of colony is pink or red and composed of erythroid cells in various stages of differentiation. Although A-MuLV is required to induce the erythroid colonies, and at least some cells in all of these colonies are infected with the virus, no permanently growing cell lines have been established from the cells in these colonies. The frequency of the two types of colonies varies depending upon the tissue and the gestational age of the embryo. Erythroid colonies are found following infection of early and mid gestation tissues while lymphoid colonies are found following infection of mid and late gestation tissues. Mixing experiments indicate that the two types of colonies arise from distinct target cells. Because A-MuLV mutants that are defective for lymphoid cell transformation are also defective for erythroid colony induction, expression of a functional Abelson protein is probably required for colony induction. Thus A-MuLV is capable of stimulating the cells of two distinct hematopoietic lineages. In one case, infection leads to transformation, while in the second, it leads to growth and differentiation. Both types of interaction are mediated, at least in part, by the same A-MuLV gene product, a molecule previously considered to induce transformation in all stably infected cells.

journal_name

Cell

journal_title

Cell

authors

Waneck GL,Rosenberg N

doi

10.1016/0092-8674(81)90035-0

subject

Has Abstract

pub_date

1981-10-01 00:00:00

pages

79-89

issue

1 Pt 1

eissn

0092-8674

issn

1097-4172

pii

0092-8674(81)90035-0

journal_volume

26

pub_type

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