Embryo Gene Activation - Essay Example

Embryonic genes, which are active prior to the 4-cell stage, are small in number and they code for proteins used in controlling and stabilizing maternal mRNA and proteins. Parental proteins regulated at the post-translational glassy by adjusting the proteins phosphorylation form. Alternatively, these protein states created by the embryonic kinases can stimulate the activities of proteins and change their cell location. For embryo development, change and degradation of maternal mRNA proteins are crucial just before the embryo gene activation.

This paper discusses embryo gene activation, DNA repair and the pathways involved in the processes (Lauritzen 240). During the 4-cell phase of embryo gene activation, remodeling of chromatin, which allows transcription of the embryo, and hence synthesizing the translation machinery. The genome of embryos becomes active and starts transcription of metabolic, apoptosis and cell cycle protein regulation (Khanna &Yosef 119). The proteins for maternal mRNAs continuously reduce in the early phases of the 4-cell phase.

Signaling pathways for embryonic gene activation example is the hedgehog signaling. The signaling pathway that transfers information to embryonic cells helps for right development. Each part of the embryo can contain different concentrations of these signaling proteins. Not only in embryonic cell development, this kind of pathway has a bigger role in adults and malfunction can cause diseases like, basal cell carcinoma. This signaling pathway is a focus regulator in most animals’ growth (Song & Lee 48).

In some other animals, lack of this pathway can lead to poor development of the brain, lungs, and the skeleton. Hedgehog signaling is crucial in regulating the maintenance and regeneration of most adult cells and tissues. Pharmaceutical companies have associated this pathway as a cause of cancer and developed drugs to cure the signaling causing diseases (Polin, William, & Steven 58). Breast cancer susceptibility gene 1 (BRCA1) and BRCA2 are genes which suppress tumor and the mutant phenotypes that predispose to both ovarian and breast cancers.

These proteins are involved in most cellular processes and contribute DNA repair and regulation in response to the damage of DNA (Ensley 113). BRCA proteins protect the genome from damage by providing maintenance of the stability of chromosomes. The big number of cellular proteins, which interact with the BCRA, propels most functions of the BRCA proteins and their functions linked to different phosphorylation events. Reasons why these proteins cause both ovarian and breast cancer are unknown today (Knobil, Jimmy & Neill 69).

These proteins are present in breast cells where they help repair the damaged DNA or destroy the cells in cases where the DNA is unrepaired body (Alpi, Pasierbek, Gartner & Loidl 16). Damaging the BRCA1 by any chance causes the damaged DNA not repaired and this may increase the chances of cancer. Most mammals have complex mechanisms to monitor damage of DNA and the required responses to maintain their integrity and repair. Some of the mechanisms for detection, repair, and cell cycle arrest to prevent damage from gametes or embryo cells (Gordon 670).

The repair of the DNA in these newly formed embryos relies on the mRNA proteins from prior ovulation. These repair genes developed in the early stages of the animal development need to be enough to equip the embryo with the maternal products for the gene expression to start at the right