Even in the organisms of most basal group in evolution, genes don’t churn out proteins at random. Everything should be controlled in a manner which is tightly regulated. Gene expression must occur only at right time during development, in defined cells and for specific amount of time only, anything more or less or in wrong tissue ,can be lethal to the cell . So how does a cell know what genes to express in which tissues and for what amount of time? How does an embryo can differentiate between its head ,legs or hands for that matter? Not everything is clear how this is achieved but significant amount of research has gone in last few years to understand anterior posterior patterning in Drosophila embryo which might help us to throw some light on early development in embryo.
Several genes take part in the early embryogenesis of Drosophila. They can be broadly classified into
1) Maternal efeect genes (eg: Bicoid and nanos)
2) Gap genes (eg: Krupple ,hunchback)
3) Pair rule genes (eg: even skipped ,paired)
4) segment polarity genes (eg: Wingless ,engrailed) and
5) Homeotic/ Hox genes ( eg: Antp class and bithorax)
The maternal-effect genes, eg: bicoid and nanos, are required during oogenesis. The transcripts or protein products of these genes are deposited in the egg at fertilization, and form morphogen gradients. Morphogens are protein molecules which diffuse from their place of origin and activate various targets in a concentration dependent manner. Maternal effect genes are common, and we know they are present in humans and other mammals. Eggs contain many more informational macromolecules than just strands of DNA, and any organism above the level of a virus is going to pass information on to its progeny via the cytoplasm. However, maternal effect genes are most important in the very earliest stages of embryonic development, and defects in them are likely to be lethal. Bicoid is necessary and sufficient to induce anterior structures whereas nanos takes care of posterior structures. The maternal-effect genes encode transcription factors that regulate the expression of the gap genes.
The gap genes roughly subdivide the embryo along the anterior/posterior axis. The gap genes are zygotic genes. Unlike maternal effect genes, which are transcribed from the mother’s DNA, zygotic genes are activated in the fertilized embryo and are transcribed from the zygote’s DNA. The gap genes in Drosophila get their name from the observation that mutations in these genes knock out, or cause a gap, in the body plan when you lose the gap gene kruppel, for instance, and a piece of the embryo’s middle fails to develop.
Eg: hunchback (hb), huckebein (hkb), tailless (tll), giant (gt), Kruppel (Kr), and knirps (kni).
The gap genes encode transcription factors that regulate the expression of the pair-rule genes
Embryogenesis in drosophila starts off in simple fashion but gets more and more complex once pair rule genes are activated by gap genes. Gap genes first activate and repress primary pair rule genes(even-skipped, hairy, and runt) Which interact with themselves and also with secondary pair rule genes (fushi tarazu, odd-skipped, paired, sloppy-paired)
The pair-rule genes divide the embryo into pairs of segments. The pair-rule genes encode transcription factors that regulate the expression of the segment polarity genes ( engrailed,wingless). The segment polarity genes set the anterior/posterior axis of each segment. The gap genes, pair-rule genes, and segment polarity genes are together called the segmentation genes, because they are involved in segment patterning.
Eric Wieschaus and Christiane Nusslein-Volhard have identified crucial steps in the early development of the organism. Specifically, they have identified major genes involved in setting up the initial axes of the embryo and its germ layers and there by setting the stage for groups of master control genes (HOX GENES) that then program the final body plan of the organism
But what makes one segment different from another and from here Hox genes take over.
The products of hox genes are transcription factors that specify segment identity by activating multiple gene expression events.
The genes are initially activated imprecisely by the concentration gradients of gap gene products.
e.g. Ubx is switched on between certain concentrations of hunchback to give a broad band of expression near the middle of the embryo. Later, fushi tarazu and even skipped sharpen the limits of Ubx expression which comes into register with the anterior boundaries of specific parasegments.