Cilia Function

What do spindle fibers do during anaphase of mitosis? Discuss both the walk and reeled-in mechanisms.

Before you buy cilia and flagella it is important to understand their functions and structures. Both cilia and flagella are whip-like columns of microtubules, covered in a membrane. They serve to move liquids across or over the surface of a cell, and can also be used to transport the cell from point A. To point B. There are 3 different types of flagellum, and 2 different types of cilia.

The ookinete is an elongated motile cell that possesses secretory organelles called micronemes that contain proteins involved in motility, tissue traversal, and invasion. A NIMA (never in mitosis/Aspergillus)-related protein kinase (Nek-4) is crucial for the development of ookinetes from zygotes (Reininger et al., 2005). The micronemal proteins CDPK3 (calcium-dependent protein kinase 3) (Ishino et al., 2006) and CTRP (circumsporozoite and TRAP-related protein) are involved in motility and infectivity of the ookinete (Dessens et al., 1999). Targeted disruption of CTRP drastically reduced the gliding motility of ctrp ookinetes and abolished the midgut epithelium infectivity and no oocysts were seen produced in vivo study (Yuda et al., 1999). Similarly, targeted disruption of CDPK3 generated mutant ookinetes that were immotile and failed to invade the midgut epithelium in vivo (Siden-Kiamos et al., 2006). For the successful invasion of midgut epithelium by the ookinete, they must attain gliding motility before to shift any cellular transformation. (Baum et al., 2006)

During prophase the spindle fibers are developed and moving towards opposite poles. During metaphase the chromatids aligns at the plane of the cell equator. During anaphase, the paired sister chromatids are separated and each move towards one pole, at this point the cohesin at the centromere are removed. Cohesin, a protein complex, plays an essential role during this process. The core subunits of the cohesin complex are: Smc 1 and 3 (structural maintenance of chromosome (5)), Rad21, and Scc 2-4 (adherin factor) which form a ring-like structure that performs cohesion on the sister chromatids in S phase and is maintained until metaphase (4). The Smc proteins contain ATPase (ABC type) at the terminal domains separated by a coiled coil domains and hinge domains which allows for interaction between the N- and C-terminals which are bridge by a heterodimer (Rad21 and Scc3 complex) (1). Cohesion process requires the Smc proteins to have the hinge domain, and ATPase activity in order for cohesin to associate with chromatin during the G1-phase (1,4). The Scc2-4 complex is required to load the cohesin complex onto chromatin (6). Scc complexes are used to mediate protein-protein interactions essential for cell division. Depletion in the protein results in severe premature sister chromatid separation (PCS) that will be discussed later (7). Once cohesion is established, Pds5 complex serves to maintain the sister chromatid structure through the G2-phase

Menin acts as an adaptor protein regulating multiple pathways involved in differentiation, DNA repair, proliferation and epigenetic modification. It is also expressed in all adult tissues which strongly indicates a key role in cell cycle regulation. This is emphasised by the fact that MEN1 knockout mice(12) die in utero with neural, hepatic and cardiac abnormalities. However, there is still a mystery to why the absence of a functioning ubiquitous protein only causes proliferation in endocrine tissue. This is partially answered by the mechanism of menin. In p27kip and p18ink4c double knockout mice(13), the mice develop parathyroid and pituitary adenomas. In other words, a very similar picture to MEN1. This is highly suggestive of menin working upstream of other cell cycle regulators, such as p27kip and p18ink4c. It also indicates that in endocrine cells there are no mechanisms to compensate for deficiency in functional menin, whilst in other tissue types can compensate. This explains why menin deficiency seems to result in endocrine

Birt-Hogg Dubé (BHD) syndrome is a rare autosomal dominant condition that’s characterized by the development of benign skin tumors and lung cysts. Moreover, these manifestations increase patients’ risk to develop renal cell carcinoma (RCC) and/or pneumothorax. Germline mutations in the Folliculin (FLCN) gene are responsible for patients to express the clinical hallmarks of BHD. Most of the BHD patient population contain mutations in the FLCN gene at exon 11, a disease-causing mutational hotspot. Research has shown mutations in FLCN are predicted to cause truncations of the gene resulting in its loss-of-function, resembling the function of a tumor suppressor. Furthermore, BHD clinical hallmarks are similar to the clinical manifestation caused by mutations in tumor suppressor, TSC1/2, such as: facial hamartomas and RCC. Although FLCN is predicted to be a tumor suppressor, the exact function of FLCN still remains unknown.

In about a third of primary ovarian tumour, EEF1A2 is raised in copy number, and whilst EEF1A2 mRNA is not measurable in normal ovarian epithelium, the rate of EEF1A2 mRNA is increased in a third of ovarian tumours. It appears here that EEF1A2 is an important ovarian cancer oncogene (Lee, 2003). Moreover, when the eEF1A2 expression is induced in human ovarian cell line, the eEF1A2 expressing cell line is more tumorigenic; this proves that eEF1A2 promotes malignancy in ovarian cells (Anand et al., 2002). EEF1A2 is also an oncogene in lung adenocarcinoma (Li et al., 2006). And in a high proportion of pancreatic carcinoma, eEF1A2 is up-regulated while it is just a little bit expressed in normal pancreas (Cao et al., 2009). EEF1A2 over-expression seems to enhance cell growth, proliferation, motility, survival and invasion of pancreatic cancer cells (Cao et al., 2009). In two third of breast cancer, EEF1A2 is over-expressed, which indicates that eEF1A2 might be an oncoprotein (Tomlinson et al., 2005). But interestingly, it has been shown that eEF1A2 also augurs

Cell cycle progression is orchestrated by a complex convergence of many signaling pathways. The decision to activate particular pathways while inhibiting others is mediated by a select group of gatekeeping proteins. At the molecular level, one particular interesting area of research is identifying particular proteins that function as crossroads of t

After the neural tube forms, the cells’ fates are determined and neurogenesis occurs. Often, this neurogenesis/ cell fate determination stage overlaps with migration. Cell fate determination is regulated by many factors, including extrinsic signaling, intrinsic signaling, location/cell migration pathway, and timing of differentiation. One example of extrinsic signaling is notch signaling. In a proneural cluster, there is initially an equal amount of notch and delta signaling. However, one cell starts expressing a higher amount of delta. This signals the other cell to express a lower amount of delta. The imbalance in signaling is amplified. The cell with a higher amount of delta signaling becomes specified as a neuroblast, and the cell that has higher

One of these genes is p53 which helps to control apoptosis and the cell cycle.3 In sarcomas p53 complexes with MDM2 which causes p53 to lose its normal function.3 In neurofibrosarcomas, a mutation of the NF-1 gene can inhibit tumor suppression.3 In almost all forms of sarcomas the lack of expression of FUS1 occurs.4 Another common tumor suppressor gene that is down regulated in various sarcomas is

It does not appear to be oncogenic by itself but it acts as suppressor of apoptosis and elevated levels have been associated proliferation and growth in normal and cancer cells (K. Ahmed 2009). CK2 appears to play an important role in memory and learning (Giraultet al. 1990) .

Centriole - these two features made of hollow tubules play a key role in cell division.

In a normal cell, the rate at which the normal cell grows and proliferate is tightly regulated, however, resistance to such regulation as a result of gene mutation is a hallmark of cancer. Proto-oncogenes, tumor suppressor genes, and microRNA genes are the three major groups of normal cellular genes associated with cancer(Faguet, 2015).

Microtubules are assembled at the microtubule organizing center (MTOC), which consist of centrosomes surrounded by pericentriolar material (PCM) in animal cells. Nucleation, which is the initiation of microtubules, occurs at the MTOC and consists of 13 gamma-tubulin subunits forming an open ring where the first set of tubulin are added at the positive end (Tassins and Bornens, 1999). Growth of the microtubule consists of the polymerization, addition of tubulin dimers on the positive end near the cell periphery, faster than tubulin dimers can be lost at the minus end, which is attached to the centrosome toward the cell center.

Cilium plays a significant role in the cause of PKD. Cilia are microtubules located on the surface of most eukaryotic cells. There are two different kinds of cilia. The first one is the motile-cilia and the second is the non-motile-cilia or ‘primary’. Motile-cilia mostly help with movement. They mostly found on the respiratory tract and middle ear. Also they help push sperm. In the other hand the non-motile-cilia are working as a sensory antenna for the cells as well as signaling between cells. Non-motile-cilia act as sensory for the concentrations of calcium flow and growth factors. In addition, the non-motile-cilia in the kidney called kidney tubules. As seen in PKD, an irregularity of non-motile cilia is the cause of abnormal cell