STRESS RESPONSES IN THE AVIAN EARLY EMBRYO - REGULATION BY PRO-APOPTOTIC AND ANTI-APOPTOTIC CELL-DEATH GENES

The avian embryo within the newly oviposited egg may be subjected to v arious environmental stresses that result in aberrant or completely in terrupted development during incubation. Although the egg itself provi des some protection against insults, it is not sufficient to protect a gainst all types of exposures or agents that are readily deposited in the egg during maturation or after fertilization. Recent research from the emerging area of apoptotic cell death sheds new light on the cell ular pathways and particular mechanisms that regulate the ultimate bio logical responses to stress. This review discusses and evaluates studi es concerning embryo mortality, environmental stress effects on early developmental progression, cellular mechanisms in stress-induced aberr ant and arrested development, and regulation of cell viability by apop totic cell-death genes. Classical and recent studies show that the avi an early embryo, at stages preceding gastrulation, is generally resist ant to stress factors such as cold and heat shock, radiation, and chem icals. This resistance tends to decline with advancing embryo age. How ever, a subset of early embryos either fail to develop normally or sho w sensitivity to stress factors. Recent studies show that pluripotent blastodermal cells are capable of undergoing apoptosis. The amount of apoptosis is increased by exposure to potent drugs and heat shock. How ever, the actual induction of apoptosis is delayed from the time of st ress exposure to the actual appearance of the apoptotic cell-death phe notype. A few 'susceptible' embryos show more rapid and extensive apop tosis induction. The basis for this apparent resistance of the early e mbryo to potent stresses may be related to the presence of multiple an ti-apoptotic gene products, such as bcl-2, hsp70, and grp78, providing protection during cleavage stages (maternal messages) and later in de velopment (embryo-derived messages). It is hypothesized that aberrant expression of cell-death regulatory genes induces death or increases s ensitivity to stresses in some embryos. Reproductive efficiency may be improved in the future through the strategy of modulating apoptosis i n the egg or early embryo.