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Husain, Z.

Publications and source records attributed to Husain, Z..

2 recordsLinked to original sources

The flavor enhancer maltol increases pigment aggregation in dermal and neural melanophores in Xenopus laevis tadpoles

Melanophores are pigmented cells that change the distribution of pigmented melanosomes, enabling animals to appear lighter or darker for camouflage, thermoregulation, and UV-protection. A complex series of hormonal and neural mechanisms regulates melanophore pigment distribution, making these cells a valuable tool to screen toxicants as a dynamic cell type that responds rapidly to the environment. We found that maltol, a naturally occurring flavor enhancer and fragrance agent, induces melanophore pigment aggregation in a dose-dependent manner in Xenopus laevis tadpoles. To determine if maltol affects camouflage adaptation, we placed tadpoles into maltol baths situated over either white or black background. Maltol induced pigment aggregation in a similar dose-dependent pattern regardless of background color. We also tested how maltol treatment compares to melatonin treatment and found that the degree of pigment aggregation induced by maltol is similar to treatment with melatonin, but the time course differs significantly. Last, maltol had no effect on mRNA expression of pro-opiomelanocortin or melanin concentrating hormone receptor in the brain, both of which regulate camouflage-related pigment aggregation. Our results suggest that maltol does not exert its effects via the camouflage adaptation mechanism nor via melatonin-based mechanisms. These results are the first to identify a specific toxicological effect of maltol exposure and rules out several mechanisms by which maltol may exert its effects on pigment aggregation.

pharmacology and toxicology

Axonal transport of an insulin-like peptide mRNA promotes stress recovery in C. elegans

Aberrations in insulin or insulin-like peptide (ILP) signaling in the brain causes many neurological diseases. Here we report that mRNAs of specific ILPs are surprisingly mobilized to the axons of C. elegans during stress. Transport of the ILP ins-6 mRNA to axons facilitates recovery from stress, whereas loss of axonal mRNA delays recovery. In addition, the axonal traffic of ins-6 mRNA is regulated by at least two opposing signals: one that depends on the insulin receptor DAF-2 and a kinesin-2 motor; and a second signal that is independent of DAF-2, but involves a kinesin-3 motor. While Golgi bodies that package nascent peptides, like ILPs, have not been previously found in C. elegans axons, we show that axons of stressed C. elegans have increased Golgi ready to package peptides for secretion. Thus, our findings present a mechanism that facilitates an animals rapid recovery from stress through axonal ILP mRNA mobilization.

neuroscience