Physiology of Mullerian Inhibiting Substance (Research Paper Sample)

Running head: Physiology of MIS (Mullerian Inhibiting Substance)
Physiology of MIS (Mullerian Inhibiting Substance)
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Physiology of MIS (Mullerian Inhibiting Substance)
This paper is insightfully going to look at the Mullerian Inhibiting Substance (MIS). What it is, its discovery, its identity, isolation, the genetics behind it, the sequence it takes, its biological properties, physiological role, disorders as well as its use as a tool in prenatal and post natal development. It is going to look into the possibilities of using MIS as a therapeutic agent to treat certain types of malignancies.
The Mullerian Inhibiting Substance (MIS) is the gonadal hormone that causes the relapse of the Mullerian ducts, it is also the anlagen of the female internal reproductive structures for the period of male embryogenesis. It is one of the members of the transforming growth factor –β (TGFβ) multigene family of glycoproteins that take part in the control of growth and differentiation. The proteins of this gene family are all formed as dimeric precursors which later undergo posttranslational processing for them to be activated. This process requires cleavage and dissociation to discharge bioactive C-terminal fragments (Lee & Donahoe, 1993).
MIS first discovery was in 1947 by a scientist A. Jost. He discovered that there was a
substance that induced the regression of the Mullerian duct during embryogenesis, the same
substance possessed a broad spectrum of activity that was involved in the inhibition of oocyte
and spermatogonium maturation, it also took part in the differentiation of gonads. Various
methods are used to isolate this hormone. During case study isolation was tried using the
Chinese hamster. Various chemical processes were done and the final residue MIS was
obtained. Its purity and homogeneity were analyzed through electrophoresis. The resultant
MIS had protein standards in the range of 20-97kD used for molecular mass determination
(Rodina et al, 2008).
MIS is genetically comprised of protein material. Analysis show that it constitutes of different kinds of amino acids in its makeup. MIS takes a certain sequence in its functioning. It starts by binding with the transmembrane type II receptor (MISR II) which after binding a heterodimer complex is formed with the type I receptor (MISR I). This step is followed by trans phosphorylation of MISR I with the MISR II receptor at a GS-site localized in the cytoplasm. Activation of the MSIR I lead to phosphorylation of receptor specific smad proteins which in-turn binds with the Smad 4 co-activator. This complex is then translocated in the nucleus and participates in regulation of gene expression. Biologically MIS is used in the specification of gender during embryology. Physiologically its role is to help distinguish between male and female properties (Rodina et al, 2008).
MIS has various disorders that are associated with it. In the case where it is in excess during early embryogenesis, it has vital effects in both males and females. In female transgenic mice for instance a production of excess MIS leads to its external genitalia being severely affected. The vagina ends without an opening, the uterus and oviducts are absent and the gonads have cordlike structures that lack germ cells. In males the external genitalia become more feminine, organs are underdeveloped and lastly the testes are undescended containing only a few germ cells (Forest, 1997).
Its presence in early fetal development contrasts with its ineffectiveness in postnatal life in both males and females and thus can candidly be used as a tool as portrayed in experiments carried out in nature. Males who have the müllerian duct syndrome, a rare form of pseudohermaphroditism characterized males having a uterus and fallopian tubes,...