Constitutive and basal secretion from the endocrine cell line, AtT-20

Analysis of the secretory process is made easier when secretion-defective mutants are available. The steps involved in constitutive secretion have been elucidated in yeast using temperature-sensitive secretion mutants (Novick et al., 1980; Schekman, 1985) . In mammalian cells, mutants have been described that influence secretion, but most of these mutations involve changes in the structure of the secretory protein itself, or changes in its posttranslational modification (for review see Tartakoff, 1983) . Many examples of defective secretion involve proteins that are constitutively secreted, such as immunoglobulin chains (for review see Scharff et al., 1975) or viral glycoproteins (Tufaro et al., 1987) . Mutations in the machinery of constitutive secretion are often lethal since the constitutive pathway is responsible for the normal membrane traffic vital for cell growth. Nonlethal mutations that affect the regulated secretory process have been reported for ciliated protozoa, for example in the exocytosis of trichocysts in Paramecium (Aufderheide, 1978; Lefort-Tran et al., 1981) and mucocysts in Tetrahymena (Orias et al., 1983; Maihle and Satir, 1985) . In this paper we describe a mammalian cell variant that has lost its capacity for regulated secretion.