Initial State of the Drosophila Eye before Dorsoventral Specification is Equivalent to Ventral

Dorsoventral (DV) patterning is crucial for eye development in invertebrates and higher animals. DV lineage restriction is the primary event in undifferentiated early eye primordia of Drosophila. InDrosophila eye disc, a dorsal-specific GATA family transcription factor pannier (pnr) controls Iroquois-Complex (Iro-C) genes to establish the dorsal eye fate whereas Lobe (L), which is involved in controlling a Notch ligand Serrate (Ser), is specifically required for ventral growth. However, fate of eye disc cells before the onset of dorsal expression of pnr and Iro-C is not known. We show that L/Ser are expressed in entire early eye disc before the expression of pnr and Iro-C is initiated in late first instar dorsal eye margin cells. Our evidence suggests that during embryogenesis pnr activity is not essential for eye development. We present evidence that loss of L or Ser function prior to initiation of pnr expression results in elimination of the entire eye, whereas after the onset of pnr expression it results only in preferential loss of ventral half of eye. We demonstrate that dorsal eye disc cells also become L or Serdependent when they are ventralized by removal of pnr or Iro-C gene function. Therefore, we propose that early state of the eye prior to DV lineage restriction is equivalent to ventral and requires L and Sergene function

Lobe and Serrate are Required for Cell Survival during Early Eye Development in Drosophila

Organogenesis involves an initial surge of cell proliferation, leading to differentiation. This is followed by cell death in order to remove extra cells. During early development, there is little or no cell death. However, there is a lack of information concerning the genes required for survival during the early cell-proliferation phase. Here, we show that Lobe (L) and the Notch (N) ligand Serrate (Ser), which are both involved in ventral eye growth, are required for cell survival in the early eye disc. We observed that the loss-of-ventral-eye phenotype in L or Ser mutants is due to the induction of cell death and the upregulation of secreted Wingless (Wg). This loss-of-ventral-eye phenotype can be rescued by (i) increasing the levels of cell death inhibitors, (ii) reducing the levels of Hid-Reaper-Grim complex, or (iii) reducing canonical Wg signaling components. Blocking Jun-N-terminal kinase (JNK) signaling, which can induce caspase-independent cell death, significantly rescued ventral eye loss in L or Ser mutants. However, blocking both caspase-dependent cell death and JNK signaling together showed stronger rescues of the L- or Ser-mutant eye at a 1.5-fold higher frequency. This suggests that L or Ser loss-of-function triggers both caspase-dependent and -independent cell death. Our studies thus identify a mechanism responsible for cell survival in the early eye

Tema 25: A vida

The Drosophila eye consists of a reiterative hexagonal array of photoreceptor cell clusters, the ommatidia. During normal morphogenesis, the clusters in the dorsal or ventral halves of the disc rotate 90° in opposite directions, forming mirror images across a dorsoventral equator. In the mutant nemo (nmo), there is an initial turning of approximately 45°, but further rotation is blocked. Genetic mosaic analysis indicates that the nmo gene acts upon each cluster as a whole; normal nmo function in one or more photoreceptor cells appears to be sufficient to induce full rotation. The nmo gene sequence encodes a serine/threonine protein kinase homolog, suggesting that the kinase is required to initiate the second step of rotation. In another mutant, roulette, excessive rotation through varying angles occurs in many ommatidia. This defect is suppressed by nmo, indicating that nmo acts upstream in a rotation-regulating pathway

Solid tumors of the pancreas can put on a mask through cystic change

<p>Abstract</p> <p>Background</p> <p>Solid pancreatic tumors such as pancreatic ductal adenocarcinoma (PDAC), solid pseudopapillary tumor (SPT), and pancreatic endocrine tumor (PET) may occasionally manifest as cystic lesions. In this study, we have put together our accumulated experience with cystic manifestations of various solid tumors of the pancreas.</p> <p>Methods</p> <p>From 2000 to 2006, 376 patients with pancreatic solid tumor resections were reviewed. Ten (2.66%) of these tumors appeared on radiological imaging studies as cystic lesions. We performed a retrospective review of medical records and pathologic findings of these 10 cases.</p> <p>Results</p> <p>Of the ten cases in which solid tumors of the pancreas manifested as cystic lesions, six were PDAC with cystic degeneration, two were SPT undergone complete cystic change, one was cystic PET, and one was a cystic schwannoma. The mean tumor size of the cystic portion in PDAC was 7.3 cm, and three patients were diagnosed as 'pseudocyst' with or without cancer. Two SPT were found incidentally in young women and were diagnosed as other cystic neoplasms. One cystic endocrine tumor was preoperatively suspected as intraductal papillary mucinous neoplasm or mucinous cystic neoplasm.</p> <p>Conclusions</p> <p>Cystic changes of pancreas solid tumors are extremely rare. However, the possibility of cystic manifestation of pancreas solid tumors should be kept in mind.</p

Topoisomerase II is regulated by translationally controlled tumor protein for cell survival during organ growth in Drosophila.

Regulation of cell survival is critical for organ development. Translationally controlled tumor protein (TCTP) is a conserved protein family implicated in the control of cell survival during normal development and tumorigenesis. Previously, we have identified a human Topoisomerase II (TOP2) as a TCTP partner, but its role in vivo has been unknown. To determine the significance of this interaction, we examined their roles in developing Drosophila organs. Top2 RNAi in the wing disc leads to tissue reduction and caspase activation, indicating the essential role of Top2 for cell survival. Top2 RNAi in the eye disc also causes loss of eye and head tissues. Tctp RNAi enhances the phenotypes of Top2 RNAi. The depletion of Tctp reduces Top2 levels in the wing disc and vice versa. Wing size is reduced by Top2 overexpression, implying that proper regulation of Top2 level is important for normal organ development. The wing phenotype of Tctp RNAi is partially suppressed by Top2 overexpression. This study suggests that mutual regulation of Tctp and Top2 protein levels is critical for cell survival during organ development

Transport of Phosphate by Renal Brush Border Membrane Vesicle (BBMV) during Development - Role of the Growth Hormone-

It is well documented that plasma concentrations of Pi (inorganic phosphorus) are higher in developing subjects than in adults. In a previous study, we demonstrated that the Vmax (capacity) of the Na-Pi cotransport mechanism of the renal brush border membrane vesicles was higher in immature than mature rats. In this study, we evaluated the role of a growth hormone in the maintenance of a higher Vmax observed in immature rats. In mature rats, serum Pi, and the tubular reabsorption of Pi (TRPi) increased in the growth hormone treated animals. On the other hand, those values were not changed by growth hormone treatment in immature rats. In kinetic analysis, the Km (affinity) values were not different between the control (growth hormone-untreated) and growth hormone-treated renal brush border membrane vesicles in both immature and mature rats. The Vmax of the immature rats also was not changed by growth hormone treatment. On the contrary, Vmax increased significantly in the growth-hormone treated than the control mature rats. With the above findings, it seems that immature rats reabsorb Pi maximally even in the control state, and it is likely that a growth hormone is responsible for the phenomenon

Cell Type-Specific Responses to Wingless, Hedgehog and Decapentaplegic Are Essential for Patterning Early Eye-Antenna Disc in Drosophila

The Drosophila eye-antenna imaginal disc (ead) is a flattened sac of two-layered epithelia, from which most head structures are derived. Secreted morphogens like Wingless (Wg), Hedgehog (Hh), and Decapentaplegic (Dpp) are important for early patterning of ead, but the underlying mechanisms are still largely unknown. To understand how these morphogens function in the ead of early larval stages, we used wg-LacZ and dpp-Gal4 markers for the examination of wild-type and mutant eads. We found that the ead immediately after hatching was crescent-shaped with the Bolwig’s nerve at the ventral edge, suggesting that it consists of dorsal domain. In a subsequent step, transcriptional induction of dpp in the cells along the Bolwig’s nerve was followed by rapid growth of the ventral domain. Both Wg and Hh were required for the formation of the ventral domain. Wg was crucial for the growth of the entire ead, but Hh was essential for cell division only in the dorsal domain. In the ventral domain, Hh regulated dpp transcription. Based on these data, we propose that signaling among distinct groups of cells expressing Wg, Dpp, or Hh in the ead of the first-instar larvae are critical for coordinated growth and patterning of ead