Research has shown that companies receiving qualified opinions report later than companies receiving unqualified opinions (see, e.g., Dodd et al. [1984] and Elliott [1982]). Audit-related reasons for this phenomenon could include an increase in the scope of the auditing procedures applied in such circumstances, as well as an increase in the amount of auditor-client negotiation time required (Whittred [1980]).

Abstract. We examine the determinants of "audit delay," the number of calendar days from fiscal year-end to the audit report date. A descriptive model of audit delay is tested on a sample of 465 companies listed on the Toronto Stock Exchange from 1977 to 1982. Although several variables included in the model are statistically significant, the proportion of variability in audit delay explained by the variables is low. Descriptive data are presented for variables consistently associated with audit delay over the six-year periodauditor size, industry classification, existence of extraordinary items, and sign of net income. Some directions for friture research are also suggested.

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MAP kinases (MAPKs), which control mitogenic signal transduction in all eukaryotic organisms, are inactivated by dual specificity MAPK phosphatases (MKPs). MKP-3, a prototypical MKP, achieves substrate specificity through its N-terminal domain binding to the MAPK ERK2, resulting in the activation of its C-terminal phosphatase domain. The solution structure and biochemical analysis of the ERK2 binding (EB) domain of MKP-3 show that regions that are essential for ERK2 binding partly overlap with its sites that interact with the C-terminal catalytic domain, and that these interactions are functionally coupled to the active site residues of MKP-3. Our findings suggest a novel mechanism by which the EB domain binding to ERK2 is transduced to cause a conformational change of the C-terminal catalytic domain, resulting in the enzymatic activation of MKP-3.