Stellar Drive Clone Serial Key

Stellar Drive Clone is a user-friendly software that allows creating clones of Mac hard drives to create a bootable copy of your system. You can also use the tool to image any volume or the entire hard drive for backup purpose. The image file created can be used to restore data in the event of a disaster. You can use the software to restore a volume from its image or the folder containing its clone. Stellar Drive Clone provides you an easy platform to create a full system backup consisting of the operating system and the installed software. The Mac hard drive cloning tool performs a comprehensive scan of the storage media sector by sector to create an exact replica or boot drive. The process involves copying hidden as well as in-use files that are excluded by normal copy methods. With this utility, you can choose to resize volumes on the destination drive according to your requirement for maximum use of disk space. You can also image your volumes or drives containing bad sectors and showing continuous erratic behavior. The image created by Stellar Drive Clone can be used to restore data in critical instances of hard drive crash. With the support for exFAT file system, you can easily clone all exFAT formatted flash drives. Further, you can clone an NTFS formatted drive to exFAT formatted drive in Mac OS X Lion. The software possesses an easy-to-use interface that empowers you to perform hard drive cloning without the risk of losing data. The tool preserves the integrity of your precious data during the process and gives you an image that exactly replicates the source drive. You have the option to set desired preferences to customize the process, such as 'Play Sound', 'Send system to sleep', or 'System Shutdown'. You can also create a minimal system that comprises Apple's default applications, files and folders on your desktop, and all the selected applications. Moreover, you can create a bootable DVD if you are suspecting a hard drive crash or system failure in future.

Stellar Drive Clone serial key

Please give us the last three figures of your serial number. I would drag off as many files as possible BEFORE attempting a disk repair as you may try to repair the disk and then find it unmountable. This may also be a bad HD/IR cable problem and can destroy the hard drive.

EGF receptor Effects of Mutation or Deletion Table of contents Egfr and oogenesis Gurken signals from the oocyte to the adjacent follicle cells twice during Drosophila oogenesis; first to induce posterior fate, thereby polarizing the anterior-posterior axis of the future embryo and then to induce dorsal fate and polarize the dorsal-ventral axis. Gurken is here shown to induce two different follicle cell fates because the follicle cells at the termini of the egg chamber differ in their competence to respond to Gurken from the main-body follicle cells in between. Anterior follicle cells are known to become subdivided into three distinct follicle cell types along the anterior-posterior axis: border cells, stretched follicle cells and centripetal follicle cells. The border cells are a group of 6-10 cells that delaminate from the follicular epithelium at the anterior tip of the egg chamber and migrate between the nurse cells to the anterior of the oocyte. At the same time, the adjacent stretched follicle cells spread to cover the nurse cells as the rest of the follicular epithelium moves posteriorly to envelop the oocyte. The centripetal follicle cells just posterior to the stretched follicle cells come to lie over the anterior of the oocyte after these movements are complete, and these cells then migrate between the oocyte and the nurse cells toward the center of the egg chamber during stage 10b (Gonzalez-Reyes, 1998). It is argued that the terminal follicle cell populations (consisting of both anterior and posterior follicle cell populations) are equivalent prior to gurken signaling. To explain how Gurken can induce two different follicle cell fates, it has been proposed that the follicle cell layer is divided into two cell types during early oogenesis: the terminal follicle cells at each end of the egg chamber, which become posterior if they receive the Gurken signal and anterior if they do not, and the main-body follicle cells, which are induced to become dorsal rather than ventral. The Egfr, as receptor of the posterior Gurken signal, is required cell autonomously to repress anterior fate in all posterior follicle cells. Although the expression of several markers at the termini of developing egg chambers suggests the existence of populations of terminal follicle cells, it is not clear how many cells respond to Gurken directly by adopting a posterior rather than an anterior fate. To define this population, a mapping was performed to determine which cells revert to the default anterior fate when they cannot respond to Gurken because they lack its putative receptor. Small marked clones of cells were generated that are homozygous for top CO, a null allele of the Egfr, and their fate was followed by staining for the beta-gal activity of the L53b enhancer trap line, which labels all three subpopulations of anterior follicle cells from stage 9 onwards. When the clones are generated (at approximately stage 2 of oogenesis) and scored at stage 10, mutant cells that lie near the posterior of the oocyte are seen to always express L53b, whereas clones over the middle of the oocyte do not. Thus, removal of the Egfr causes a cell-autonomous transformation from posterior to anterior fate, indicating that Gurken signals directly to induce posterior fate in the whole terminal follicle cell population. With one exception, all Egfr- cells that fall within 10-11 cell diameters of the posterior end of the egg chamber express L53b, whereas mutant cells that fall anterior to this boundary do not. This analysis indicates that about 200 terminal follicle cells receive the Gurken signal directly, ruling out a model in which only the polar follicle cells (the most posterior cell population) are competent to respond to Gurken by becoming posterior. The cells that become anterior if they cannot respond to Gurken constitute the entire population of follicle cells that contact the oocyte during previtellogenic stages. Thus, all of the cells that receive the posteriorizing Gurken signal are competent to respond to it (Gonzalez-Reyes, 1998). In mutants such as gurken in which the induction of posterior follicle cell fate is blocked, the terminal follicle cells at the posterior develop like their anterior counterparts by forming border, stretched and centripetal follicle cells. This raises the question of whether the anterior follicle cells are subdivided into three cell types after the decision between anterior and posterior is taken, or whether there is a symmetric prepattern in the terminal follicle cells at both ends of the egg chamber. The ability to generate small clones of anterior cells at the posterior by removing the Egfr makes it possible to distinguish between these possibilities. If the latter model is correct, isolated patches of anterior cells should still respond to the symmetric prepattern correctly and form the appropriate type of anterior cell, even though they are surrounded by posterior cells, whereas the former model predicts that these cells should be unable to interpret their position. To follow the fate of small patches of anterior cells at the posterior of the egg chamber, small Egfr- clones were generated, but in this case, clone generation took place in the presence of enhancer trap lines that are expressed specifically in each of the three anterior follicle cell types. Egfr- cells that fall within a region 8-11 cell diameters from the posterior pole show staining for a centripetal cell marker, whereas clones that fall either proximal or distal to this 3-cell-wide belt do not activate this marker. Thus, anterior cells at the posterior express the anterior BB127 centripetal cell marker autonomously in a region that is the exact posterior counterpart of the anterior centripetal follicle cell domain. Furthermore, clones of as few as 4 cells express BB127 if they fall within this region, indicating that anterior cells can correctly interpret their position with respect to the posterior pole, although all of the surrounding cells are posterior. The same conclusion applies to a border cell and a stretched cell marker. The results demonstrate that small posterior clones of anterior cells can interpret their position with respect to the posterior pole by adopting the appropriate anterior follicle cell fate: the most terminal Egfr- cells behave like border cells, the subterminal Egfr- cells behave like stretched follicle cells, and the least terminal like centripetal cells. Thus, the positional information that specifies the positions of these distinct cell types at the anterior pole is also present at the posterior, strongly suggesting that there is a symmetric prepattern within the terminal follicle cell population that is independent of the decision between anterior and posterior fate (Gonzalez-Reyes, 1998). These results suggest a three-step model for the anterior-posterior patterning of the follicular epithelium that subdivides this axis into at least five distinct cell types. Altogether, these observations support a stepwise model for the patterning of the follicle cell layer along the AP axis. In the first step, the follicle cell epithelium is divided into terminal and main-body follicle cell populations. There is no lineage restriction boundary between the posterior terminal follicle cells and the main-body follicle cells at a stage in development that is four cell divisions before stage 6, indicating that the distinction between these two cell types arises after stage 1. Because the terminal cells have to be specified before Gurken signaling occurs, this restricts the time at which this population is determined to between stages 2 and 5. Although the data do not suggest a mechanism for how these cells are specified, their position suggests a simple model in which they are induced by a terminalizing signal that spreads from the two poles of the egg chamber. The most likely sources for such a signal are the two polar follicle cells at each end of the egg chamber, since these cells lie in the center of the terminal domain and adopt a terminal fate themselves. The next step in the patterning of the follicular epithelium is the formation of a symmetric prepattern within each terminal follicle cell population. How this prepattern is established is unknown, but the geometry of the egg chamber again suggests that it might involve signals that emanate from the poles. Indeed, it is possible that the terminal follicle cells are specified and patterned by the same process, since both events require Notch activity. For example, the terminalizing signal could induce distinct terminal fates at different distances from the pole. The third step in the patterning of the follicle cell layer occurs when the oocyte induces one population of terminal follicle cells to adopt a posterior fate, thereby breaking the symmetry of the follicle cell layer. As a consequence, the symmetric prepattern in the terminal follicle cells is interpreted differently in the anterior and posterior populations. The anterior cells become subdivided into border, stretched and centripetal follicle cells, while the posterior cells may undergo a similar subdivision into posterior cell types. In this way, the sequential patterning of the terminal follicle cells gives rise to at least five different cell types along the anterior-posterior axis (Gonzalez-Reyes, 1998). During Drosophila oogenesis the body axesare determined by signaling between the oocyte and thesomatic follicle cells that surround the egg chamber. Akey event in the establishment of oocyte anterior-posteriorpolarity is the differential patterning of the follicle cellepithelium along the anterior-posterior axis. Both theNotch and epithelial growth factor (EGF) receptor pathwaysare required for this patterning. To understand howthese pathways act in the process, an examination was made using markers for anterior and posterior follicle cells accompanyingconstitutive activation of the EGF receptor, loss ofNotch function, and ectopic expression of Delta. A constitutively active EGF receptor can induce posteriorfate in anterior but not in lateral follicle cells,showing that the EGF receptor pathway can act only onpredetermined terminal cells. Furthermore, Notch functionis required at both termini for appropriate expressionof anterior and posterior markers, while loss of boththe EGF receptor and Notch pathways mimic the Notchloss-of-function phenotype. Ectopic expression of theNotch ligand, Delta, disturbs EGF receptor dependentposterior follicle cell differentiation and anterior-posteriorpolarity of the oocyte. These data are consistent with amodel in which the Notch pathway is required for earlyfollicle cell differentiation at both termini, but is then repressedat the posterior for proper determination of theposterior follicle cells by the EGF receptor pathway (Larkin, 1999).To further investigate the interplay between Notch andDelta in follicle cell differentiation the effectof overexpression of Delta in the germarium was studied. The Drosophilaovary consists of 15-20 ovarioles: strings of eggchambers aligned in developmental order. At the anteriorend of each ovariole lies the germarium, where the germline stem cells divide to form 16 cell cysts. These cystsare enveloped by a somatic follicle cell layer and releasedfrom the germarium as a subset of follicle cellsintercalates to form an interfollicular stalk. Expression of constitutively activeNotch generates long stalks in the germarium by virtueof holding the stalk cells and polar cells in a precursorstage. Loss of Notch or Delta activityresults in the opposite phenotype: lack of stalks.Overexpression of Delta in the germarium leads to theformation of long stalklike structures. Theselong stalks do not contain differentiated stalk or polarcells. Instead the markers Fasciclin III (FasIII) andBig Brain (Bib) are expressed as in the stalk cell precursors. These data suggest that overexpression of Delta produces long stalks due to a prolongedprecursor stage for stalk and polar cells, a phenotypeobserved previously due to expression of constitutivelyactive Notch; thus the phenotype produced byoverexpression of Delta mimics that of the constitutively activeNotch receptor in this developmental process (Larkin, 1999).The data presented here show that the function of theEGF receptor pathway in posterior follicle cells requiresfunctional Notch, but that the Notch pathway can act inthese cells without an active EGF receptor pathway. A targetfor the EGF receptor pathway, pointed P1 is not activatedin temperature sensitive Notch egg chambers, but the Notch-dependenttermini are established in grk mutants. In addition, inNotch and grk double mutant experiments, the Notch loss-of-function phenotype is observed. However, ifa ligand for Notch, Delta is overproduced at stage 6, posteriorfollicle cell development is compromised. The simplestmodel to explain these data is one in which theNotch pathway acts in both termini for differentiation ofthe terminal follicle cells and is subsequently repressed atthe posterior for the EGF receptor-dependent posteriorfollicle cell differentiation. Therefore, properfunction of the EGF receptor pathway in the posterior folliclecells requires the cessation of Delta expression inthese follicle cells, suggesting that the Notch pathway canmodulate cellular responses to the EGF receptor pathway (Larkin, 1999).In Drosophila, the dorsoventral asymmetry of the egg chamber depends on a dorsalizing signal thatemanates from the oocyte. This signal is supplied by the TGF alpha-like Gurken protein whoseRNA is localized to the dorsal-anterior corner of the oocyte. Gurken protein expressed in the follicular epitheliumsurrounding the oocyte is the potential ligandof the Drosophila EGF receptor. Changes in the dorsalizing germ-line signal affectthe embryonic dorsoventral pattern. A reduction in strength of the germ-line signal as produced bymutations in gurken or Egfr does not change the slope of the embryonic dorsoventralmorphogen gradient, but causes a splitting of the gradient ventrally. This leads to embryos with twopartial dorsoventral axes (Roth, 1994). A set of dorsal follicle cells is patterned by the oocyte in a cell-cell signaling event occurring at stages 8 and 9 when the germinal vesicle (nucleus) migrates to the dorsal anterior of the oocyte. The anterodorsally positioned oocyte nucleus produces Gurken mRNA, a proposed ligand for the Epidermal growth cell receptor gene present on the overlying follicle cells. Activating Egfr transmits a signal through a Raf-dependent signaling pathway to generate anterior dorsal follicle cell fates, resulting in the respective specializations of the eggshell, including the dorsal appendages. A ventral follicle cell subpopulation that does not experience induction by Gurken produces molecular cues for a different inductive event, directing embryonic dorsal-ventral embryonic axis formation (Dobens, 1997 and references). A Drosophila sequence homologous to the mammalian growthfactor-stimulated TSC-22 gene was isolated in an enhancer trap screen for genes expressed in anterodorsal follicle cells during oogenesis. In situ hybridization reveals that bunched transcripts localize tothe anterior dorsal follicle cells at stages 10-12 of oogenesis. Additional staining is evident in the border cells at the nurse cell/oocyte border and in a group of posterior polar follicle cells. The centripetally migrating follicle cells, just anterior to the stained columnar cells of the anterodorsal patch do not stain. Changes in bun enhancertrap expression in genetic backgrounds that disrupt the grk/Egfr signaling pathwaysuggest that bun is regulated by growth factor patterning of dorsal anterior follicle cellfates. In fs(1)K10 mutant egg chambers, dorsal follicle cell fates expand at the expense of ventral follicle cell fates, presumably due to mislocalization of GRK mRNA from the anterodorsal portion of the oocyte to more ventral positions. In fs(1)K10 females, expression of bunched expands ventrally, with two maxima in the anterodorsal anteroventral follicle cells, diminishing laterally. In stage 10 follicles from Egfr mutants expression of bun is lost from the dorsal anterior; reduced bun expression is shifted to more posterior follicle cells. Egg chambers from a gurken mutant completely lack dorsal appendages. No bunched expression is seen in the dorsal anterior follicle cells from stage 10 gurken mutant egg chambers. Clonal analysis shows that bun is required for the proper elaboration of dorsalcell fates leading to the formation of the dorsal appendages. Eggs from bunched mutants are shortened and their dorsal appendages are short and often wide, with branched and split ends (Dobens, 1997). Preliminary evidence indicates the bunched is sensitive to decapentaplegic levels in the follicle cells. It is therefore thought that normal bunched expression in the dorsal anterior follicle cells is the result of combined action of the Egfr receptor for Grk and serine/threonine kinase receptors (see Thick veins and Punt) for Decapentaplegic (Dobens, 1997). The Drosophila eggshell, which has a pair of chorionic appendages (dorsal appendages) locatedasymmetrically along both the anterior/posterior and dorsal/ventral axes, provides a good model tostudy signal instructed morphogenesis. Broad-Complex, a gene encod