Does the Presence of Surplus Labor Hinder Production in Indian Manufacturing?

Input congestion occurs at a given input bundle when the assumption of free disposability of inputs does not hold and an increase in input leads to a decline in output. In this paper we employ the nonparametric method of Data Envelopment Analysis (DEA) to examine the question on input congestion with respect to labor, using state level data from the Annual Survey of Industries for the period 1986-87 through 1999-2000. When the standard assumption of strong disposability is relaxed for the labor inputs, the nonparametric analysis of state-level data from Indian manufacturing shows considerable measure of labor input congestion. While in selected states congestion comes from non-production workers as well, the principal source of labor congestion is production labor. There is no evidence that the problem of labor congestion has become less severe during the post-Reform years. It appears that market forces without any major institutional changes in enforcement of labor discipline cannot eliminate congestion.

A negative regulator mediates quorum-sensing control of exopolysaccharide production in Pantoea stewartii subsp. stewartii.

Classical quorum-sensing (autoinduction) regulation, as exemplified by the lux system of Vibrio fischeri, requires N-acyl homoserine lactone (AHL) signals to stimulate cognate transcriptional activators for the cell density-dependent expression of specific target gene systems. For Pantoea stewartii subsp. stewartii, a bacterial pathogen of sweet corn and maize, the extracellular polysaccharide (EPS) stewartan is a major virulence factor, and its production is controlled by quorum sensing in a population density-dependent manner. Two genes, esaI and esaR, encode essential regulatory proteins for quorum sensing. EsaI is the AHL signal synthase, and EsaR is the cognate gene regulator. esaI, DeltaesaR, and DeltaesaI-esaR mutations were constructed to establish the regulatory role of EsaR. We report here that strains containing an esaR mutation produce high levels of EPS independently of cell density and in the absence of the AHL signal. Our data indicate that quorum-sensing regulation in P. s. subsp. stewartii, in contrast to most other described systems, uses EsaR to repress EPS synthesis at low cell density, and that derepression requires micromolar amounts of AHL. In addition, derepressed esaR strains, which synthesize EPS constitutively at low cell densities, were significantly less virulent than the wild-type parent. This finding suggests that quorum sensing in P. s. subsp. stewartii may be a mechanism to delay the expression of EPS during the early stages of infection so that it does not interfere with other mechanisms of pathogenesis.