Animal Development- Part I

The study of development of embryo is referred as Embryology. The history of Embryology dates back to  18th century, the prevailing notion in human embryology was preformation: the idea that" semen contains an embryo — a preformed, miniature infant, or "homunculus" — that simply becomes larger during development. The competing explanation of embryonic development was epigenesis, originally proposed 2,000 years earlier by Aristotle. According to epigenesis, the form of an animal emerges gradually from a relatively formless egg. As microscopy improved during the 19th century, biologists could see that embryos took shape in a series of progressive steps, and epigenesis displaced preformation as the favored explanation among embryologist.
Modern embryological pioneers include Gavin de Beer, Charles Darwin, Ernst Haeckel, J.B.S. Haldane, and Joseph Needham, while much early embryology came from the work of Aristotle and the great Italian anatomists: Aldrovandi, Aranzio, Leonardo da Vinci, Marcello Malpighi, Gabriele Falloppia, Girolamo Cardano, Emilio Parisano, Fortunio Liceti, Stefano Lorenzini, Spallanzani, Enrico Sertoli, Mauro Rusconi, etc.]
After the 1950s, with the DNA helical structure being unravelled and the increasing knowledge in the field of molecular biology, developmental biology emerged as a field of study which attempts to correlate the genes with morphological change, and so tries to determine which genes are responsible for each morphological change that takes place in an embryo, and how these genes are regulate.
There are 5 stages of animal development:
1)      Gametogeneis
2)      Fertilization
3)      Clevage
4)      Gastrulation
5)      Organogenesis

In this section we will discuss about the process of Gametogenesis in detail:

Gametogenesis in layman terms refer to formation of gametes (an easy guess!!!), well let’s get into deeper, into the  roots and understand it, that actually gametogenesis is the process by which a diploid or a haploid  precursor cell undergoes cell division and maturation to ultimately form a functional gamete.

In plants it’s the haploid cell that forms the gametes but in case of animals it is usually a diploid cell that forms haploid gametes.
Talking specifically of Animal Embryology, Animals produce gametes directly through meiosis in organs called gonads. Males and females of a species that reproduces sexually have different forms of gametogenesis:

However, before turning into gametogonia, the embryonic development of gametes is the same in males and females
The Common Path

 Gametogonia are usually seen as the initial stage of gametogenesis. However, gametogonia are themselves successors of primordial germ cells. During early embryonic development, primordial germ cells (PGCs) from the dorsal endoderm of the yolk sac migrate along the hindgut to the gonadal ridge. They multiply by mitosis and once they have reached the gonadal ridge in the late embryonic stage, they are called gametogonia. Gametogonia are no longer the same between males and females.

p53 role in Human Cancer

The p53 gene , is a tumor suppressor gene, i.e., its activity stops the formation of tumors. If a person inherits only one functional copy of the p53 gene from their parents, they are predisposed to cancer and usually develop several independent tumors in a variety of tissues in early adulthood. This condition is rare, and is known as Li-Fraumeni syndrome. However, mutations in p53 are found in most tumor types, and so contribute to the complex network of molecular events leading to tumor formation.
The p53 gene has been mapped to chromosome 17. In the cell, p53 protein binds DNA, which in turn stimulates another gene to produce a protein called p21 that interacts with a cell division-stimulating protein (cdk2). When p21 is complexed with cdk2 the cell cannot pass through to the next stage of cell division. Mutant p53 can no longer bind DNA in an effective way, and as a consequence the p21 protein is not made available to act as the 'stop signal' for cell division. Thus cells divide uncontrollably, and form tumors.
Help with unraveling the molecular mechanisms of cancerous growth has come from the use of mice as models for human cancer, in which powerful 'gene knockout' techniques can be used. The amount of information that exists on all aspects of p53 normal function and mutant expression in human cancers is now vast, reflecting its key role in the pathogenesis of human cancers. It is clear that p53 is just one component of a network of events that culminate in tumor formation.
 The  p53 gene is often mutated in cancer with a high proportion of missense mutations, leading to the production of a protein expressed at high levels that differs from wild-type p53 by just one amino acid residue. This feature is a characteristic of p53, as many ‘classical’ suppressor genes, such as APC or BRCA1, are mainly altered through nonsense or frameshift mutations leading to the expression of inactive truncated proteins. In the few years following the p53 discovery in 1979, it was reported that missense mutant p53 might exert some oncogenic function (or gain of function (GOF)). In particular, they can cooperate with oncogenes, such as Ras, to transform primary rodent fibroblasts. For more than a decade, the most convincing observation supporting a GOF has been that mutant p53 is often expressed at high levels throughout tumor progression stages, even in distant metastases. Soon after the elucidation of the main mechanisms controlling wild-type p53 in the 1990s, the hunt for mutant p53 functions became a major goal in cancer research. Today, a large body of knowledge has accumulated on mutant p53 GOF, which appears as a major contender in human cancer.