109 research outputs found
The Effect of the Herbicide Glyphosate on the Growth of Selenastrum Capricornutum
The herbicide glyphosate (MON-0139), an isopropylamine salt of N- (phosphonemethyl)glycine, was tested to determine its effects on the growth of the fresh water green alga Selenastrum capricornutum. Experiments were carried out to determine algicidal, algistatic, and inhibitory concentrations of the compound.
Concentrations from 5 ppm to 1000 ppm were inhibitory to the growth of the alga, but the effects were algistatic, rather than algicidal. At concentrations from 0.1 ppm to 1.0 ppm the growth of the alga was stimulated by the presence of the herbicide, while at concentrations from 0.001 ppm to 0.05 ppm the effects of the herbicide were negligible.
Two chemical tests were used, and it was determined that in low pH systems (pH of about 4.5) glyphosate hydrolyzes with inorganic phosphate as one of the hydrolysis products. The concentrations of phosphate released is so low as to have no effect on the growth of S. capricornutum
Fine Structural Aspects of the Developing Eye of the Honey Bee
The post-embryonic development of the compound eye of the worker honey bee was investigated with the light and electron microscopes. The cells of the optic primordium were reorganized into preommatidial cell clusters during the late third and early fourth larval instars. Each cluster contained nine prospective retinula cells, the ninth was centrally located and shorter than the other eight; four prospective cone cells; and an undetennined number of prospective pigment cells.
Rhabdomere development began in the eight peripherally located retinula cells just prior to pupation. Following pupation, each ommatidium elongated. During ommatidial elongation, the short ninth retinula cell moved from its central location to a peripheral location within the ommatidium and also developed a rhabdomere. The shape of each prospective crystalline cone also changed from teardrop-shaped to spherical to the typical cone shape of the adult during differentiation.
The involvement of junctional specializations of membranes and of microtubules in the processes of differentiation, including elongation, cellular migration, and cellular organization, have been raised. Also, the role of multivesicular bodies in the process of lens formation has been discussed
The Met receptor tyrosine kinase prevents zebrafish primary motoneurons from expressing an incorrect neurotransmitter
Mechanisms of growth cone repulsion
Research conducted in the last century suggested that chemoattractants guide cells or their processes to appropriate locations during development. Today, we know that many of the molecules involved in cellular guidance can act as chemorepellents that prevent migration into inappropriate territories. Here, we review some of the early seminal experiments and our current understanding of the underlying molecular mechanisms
Delta-Notch signaling and lateral inhibition in zebrafish spinal cord development
BACKGROUND: Vertebrate neural development requires precise coordination of cell proliferation and cell specification to guide orderly transition of mitotically active precursor cells into different types of post-mitotic neurons and glia. Lateral inhibition, mediated by the Delta-Notch signaling pathway, may provide a mechanism to regulate proliferation and specification in the vertebrate nervous system. We examined delta and notch gene expression in zebrafish embryos and tested the role of lateral inhibition in spinal cord patterning by ablating cells and genetically disrupting Delta-Notch signaling. RESULTS: Zebrafish embryos express multiple delta and notch genes throughout the developing nervous system. All or most proliferative precursors appeared to express notch genes whereas subsets of precursors and post-mitotic neurons expressed delta genes. When we ablated identified primary motor neurons soon after they were born, they were replaced, indicating that specified neurons laterally inhibit neighboring precursors. Mutation of a delta gene caused precursor cells of the trunk neural tube to cease dividing prematurely and develop as neurons. Additionally, mutant embryos had excess early specified neurons, with fates appropriate for their normal positions within the neural tube, and a concomitant deficit of late specified cells. CONCLUSIONS: Our results are consistent with the idea that zebrafish Delta proteins, expressed by newly specified neurons, promote Notch activity in neighboring precursors. This signaling is required to maintain a proliferative precursor population and generate late-born neurons and glia. Thus, Delta-Notch signaling may diversify vertebrate neural cell fates by coordinating cell cycle control and cell specification
Delta-Notch signaling and lateral inhibition in zebrafish spinal cord development: Correction
Netrin Signaling Breaks the Equivalence between Two Identified Zebrafish Motoneurons Revealing a New Role of Intermediate Targets
We previously showed that equivalence between two identified zebrafish motoneurons is broken by interactions with identified muscle fibers that act as an intermediate target for the axons of these motoneurons. Here we investigate the molecular basis of the signaling interaction between the intermediate target and the motoneurons.We provide evidence that Netrin 1a is an intermediate target-derived signal that causes two equivalent motoneurons to adopt distinct fates. We show that although these two motoneurons express the same Netrin receptors, their axons respond differently to Netrin 1a encountered at the intermediate target. Furthermore, we demonstrate that when Netrin 1a is knocked down, more distal intermediate targets that express other Netrins can also function to break equivalence between these motoneurons.Our results suggest a new role for intermediate targets in breaking neuronal equivalence. The data we present reveal that signals encountered during axon pathfinding can cause equivalent neurons to adopt distinct fates. Such signals may be key in diversifying a neuronal population and leading to correct circuit formation
Transcriptomes of post-mitotic neurons identify the usage of alternative pathways during adult and embryonic neuronal differentiation
Original Panther analysis tool data tables showing values and p -values for overrepresentation data sets. (XLSX 21Â kb
Transcription factor Ap-2alpha is necessary for development of embryonic melanophores, autonomic neurons and pharyngeal skeleton in zebrafish
The genes that control development of embryonic melanocytes are poorly defined. Although transcription factor Ap-2a is expressed in
neural crest (NC) cells, its role in development of embryonic melanocytes and other neural crest derivatives is unclear because mouse Ap-2a
mutants die before melanogenesis. We show that zebrafish embryos injected with morpholino antisense oligonucleotides complementary to
ap-2a (ap-2a MO) complete early morphogenesis normally and have neural crest cells. Expression of c-kit, which encodes the receptor for
the Steel ligand, is reduced in these embryos, and, similar to zebrafish c-kit mutant embryos, embryonic melanophores are reduced in number
and migration. The effects of ap-2a MO injected into heterozygous and homozygous c-kit mutants support the notion that Ap-2a works
through C-kit and additional target genes to mediate melanophore cell number and migration. In contrast to c-kit mutant embryos, in ap-2a
MO-injected embryos, melanophores are small and under-pigmented, and unexpectedly, analysis of mosaic embryos suggests Ap-2a
regulates melanophore differentiation through cell non-autonomous targets. In addition to melanophore phenotypes, we document reduction
of other neural crest derivatives in ap-2a MO-injected embryos, including jaw cartilage, enteric neurons, and sympathetic neurons. These
results reveal that Ap-2a regulates multiple steps of melanophore development, and is required for development of other neuronal and nonneuronal
neural crest derivatives.This work was
supported by NIH grant HD22486 to J.S.E. and a Carver
Foundation seed grant to R.A.C. C. d’., and M.A. were
supported by grants ICM P99-137-f and Fondecyt 1031003.
E.K.O. was supported by Grant T32 DC00040 (Bruce
Gantz, PI)
Intrinsic molecular signature of breast cancer in a population-based cohort of 412 patients
BACKGROUND: Molecular markers and the rich biological information they contain have great potential for cancer diagnosis, prognostication and therapy prediction. So far, however, they have not superseded routine histopathology and staging criteria, partly because the few studies performed on molecular subtyping have had little validation and limited clinical characterization. METHODS: We obtained gene expression and clinical data for 412 breast cancers obtained from population-based cohorts of patients from Stockholm and Uppsala, Sweden. Using the intrinsic set of approximately 500 genes derived in the Norway/Stanford breast cancer data, we validated the existence of five molecular subtypes – basal-like, ERBB2, luminal A/B and normal-like – and characterized these subtypes extensively with the use of conventional clinical variables. RESULTS: We found an overall 77.5% concordance between the centroid prediction of the Swedish cohort by using the Norway/Stanford signature and the k-means clustering performed internally within the Swedish cohort. The highest rate of discordant assignments occurred between the luminal A and luminal B subtypes and between the luminal B and ERBB2 subtypes. The subtypes varied significantly in terms of grade (p < 0.001), p53 mutation (p < 0.001) and genomic instability (p = 0.01), but surprisingly there was little difference in lymph-node metastasis (p = 0.31). Furthermore, current users of hormone-replacement therapy were strikingly over-represented in the normal-like subgroup (p < 0.001). Separate analyses of the patients who received endocrine therapy and those who did not receive any adjuvant therapy supported the previous hypothesis that the basal-like subtype responded to adjuvant treatment, whereas the ERBB2 and luminal B subtypes were poor responders. CONCLUSION: We found that the intrinsic molecular subtypes of breast cancer are broadly present in a diverse collection of patients from a population-based cohort in Sweden. The intrinsic gene set, originally selected to reveal stable tumor characteristics, was shown to have a strong correlation with progression-related properties such as grade, p53 mutation and genomic instability
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