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.
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