Fluctuating asymmetry in Drosophila

Fluctuating asymmetry (FA) or subtle differences between left and right sides of a trait has been considered as an indicator of an organism's ability to cope with genetic and environmental stresses during development. It is considered to play an important role in mate choice. However, over four decades of work on various organisms such as insects, reptiles, birds and mammals has left the field with no clear-cut relationship between increased fluctuating asymmetry and stress due to inconsistency in the results. Despite this, fluctuating asymmetry is still assumed to indicate developmental instability caused by various perturbations (either genetic and/or environmental in origin) during development. The present article provides a unified framework for the better understanding of fluctuating asymmetry and its association with stress in particular reference to Drosophila

Cardiac matrix: A clue for future therapy

AbstractCardiac muscle is unique because it contracts ceaselessly throughout the life and is highly resistant to fatigue. The marvelous nature of the cardiac muscle is attributed to its matrix that maintains structural and functional integrity and provides ambient micro-environment required for mechanical, cellular and molecular activities in the heart. Cardiac matrix dictates the endothelium myocyte (EM) coupling and contractility of cardiomyocytes. The matrix metalloproteinases (MMPs) and their tissue inhibitor of metalloproteinases (TIMPs) regulate matrix degradation that determines cardiac fibrosis and myocardial performance. We have shown that MMP-9 regulates differential expression of micro RNAs (miRNAs), calcium cycling and contractility of cardiomyocytes. The differential expression of miRNAs is associated with angiogenesis, hypertrophy and fibrosis in the heart. MMP-9, which is involved in the degradation of cardiac matrix and induction of fibrosis, is also implicated in inhibition of survival and differentiation of cardiac stem cells (CSC). Cardiac matrix is distinct because it renders mechanical properties and provides a framework essential for differentiation of cardiac progenitor cells (CPC) into specific lineage. Cardiac matrix regulates myocyte contractility by EM coupling and calcium transients and also directs miRNAs required for precise regulation of continuous and synchronized beating of cardiomyocytes that is indispensible for survival. Alteration in the matrix homeostasis due to induction of MMPs, altered expression of specific miRNAs or impaired signaling for contractility of cardiomyocytes leads to catastrophic effects. This review describes the mechanisms by which cardiac matrix regulates myocardial performance and suggests future directions for the development of treatment strategies in cardiovascular diseases