SummaryHow the direction of axon guidance is determined is not understood. In Caenorhabditis elegans the UNC-40 (DCC) receptor mediates a response to the UNC-6 (netrin) guidance cue that directs HSN axon development. UNC-40 becomes asymmetrically localized within the HSN neuron to the site of axon outgrowth. Here we provide experimental evidence that the direction of guidance can be explained by the stochastic fluctuations of UNC-40 asymmetric outgrowth activity. We find that the UNC-5 (UNC5) receptor and the cytoskeletal binding protein UNC-53 (NAV2) regulate the induction of UNC-40 localization by UNC-6. If UNC-40 localization is induced without UNC-6 by using an unc-53 mutation, the direction of UNC-40 localization undergoes random fluctuations. Random walk models describe the path made by a succession of randomly directed movement. This model was experimentally tested using mutations that affect Wnt/PCP signaling. These mutations inhibit UNC-40 localization in the anterior and posterior directions. As the axon forms in Wnt/PCP mutants, the direction of UNC-40 localization randomly fluctuates; it can localize in either the anterior, posterior, or ventral direction. Consistent with a biased random walk, over time the axon will develop ventrally in response to UNC-6, even though at a discrete time UNC-40 localization and outgrowth can be observed anterior or posterior. Also, axon formation is slower in the mutants than in wild-type animals. This is also consistent with a random walk since this model predicts that the mean square displacement (msd) will increase only linearly with time, whereas the msd increases quadratically with time for straight-line motion.
The gas-phase decomposition of dimethyl methylphosphonate (DMMP) has been studied over amorphous manganese oxide (AMO) catalysts in the presence of light (∼200-800 nm). The reaction was studied under oxidizing conditions using air at low temperatures (40-70 °C). DMMP and gas-phase products were studied using gas chromatography (GC). DMMP was found to adsorb strongly to the AMO surface and produce small amounts of methanol (MeOH) even in the absence of light. When AMO was irradiated with light of ∼200-800 nm, large amounts of MeOH and CO 2 were initially formed. Following the initial period of high activity, strong deactivation was observed. After the reactions were performed, aqueous extracts from spent AMO were analyzed using ion chromatography (IC). The IC analyses indicated that several products accumulate on the AMO surface. These products include methyl methylphosphonate (MMP) and methylphosphonic acid (MPA). Greater amounts of MMP and MPA are produced after irradiation. Fourier transform infrared (FTIR) spectroscopy was used to examine adsorbed DMMP species on spent AMO. The IR results indicate that DMMP bonds to Mn Lewis acid sites on the AMO surface via the phosphoryl oxygen. On the basis of these results a mechanism is proposed for the adsorption and photoassisted decomposition of DMMP over AMO.
The zebrafish retina grows for a lifetime. Whether embryonic and postembryonic retinogenesis conform to the same developmental program is an outstanding question that remains under debate. Using single-cell RNA sequencing of ∼20,000 cells of the developing zebrafish retina at four different stages, we identified seven distinct developmental states. Each state explicitly expresses a gene set. Disruption of individual state-specific marker genes results in various defects ranging from small eyes to the loss of distinct retinal cell types. Using a similar approach, we further characterized the developmental states of postembryonic retinal stem cells (RSCs) and their progeny in the ciliary marginal zone. Expression pattern analysis of state-specific marker genes showed that the developmental states of postembryonic RSCs largely recapitulated those of their embryonic counterparts, except for some differences in rod photoreceptor genesis. Thus, our findings reveal the unifying developmental program used by the embryonic and postembryonic retinogenesis in zebrafish.
Abstract:The volatile compounds from brown millet (BM), milled millet (MM) and millet bran (MB) were extracted using simultaneous distillation/extraction with a Likens-Nickerson apparatus. The extracts were analysed using gas chromatography coupled with mass spectrometry (GC-MS). A total of 65 volatile compounds were identified in all of the samples. Among these compounds, 51, 51 and 49 belonged to BM, MM and MB, respectively. Aldehydes and benzene derivatives were the most numerous among all of the compounds. Three compounds (hexanal, hexadecanoic acid and 2-methylnaphthalene) were dominant in the BM and MM materials. Eight compounds (hexanal, nonanal, (E)-2-nonenal, naphthalene, 2-methylnaphthalene, 1-methylnaphthalene, hexadecanoic acid and 2-pentylfuran) were dominant in the MB materials. Apart from the aromatic molecules, which were present in all fractions, compounds present only in BM, MM or MB were also identified.
How extracellular molecules influence the direction of axon guidance is poorly understood. The HSN axon of Caenorhabditis elegans is guided towards a ventral source of secreted UNC-6 (netrin). The axon’s outgrowth response to UNC-6 is mediated by the UNC-40 (DCC) receptor. We have proposed that in response to the UNC-6 molecule the direction of UNC-40-mediated axon outgrowth is stochastically determined. The direction of guidance is controlled by asymmetric cues, including the gradient of UNC-6, that regulate the probability that UNC-40-mediated axon outgrowth is directed on average, over time, in a specific direction. Here we provide genetic evidence that a specialized extracellular matrix, which lies ventral to the HSN cell body, regulates the probability that UNC-40-mediated axon outgrowth will be directed ventrally towards the matrix. We show that mutations that disrupt the function of proteins associated with this matrix, UNC-52 (perlecan), UNC-112 (kindlin), VAB-19 (Kank), and UNC-97 (PINCH), decrease the probability of UNC-40-mediated axon outgrowth in the ventral direction, while increasing the probability of outgrowth in the anterior and posterior directions. Other results suggest that INA-1 (α integrin) and MIG-15 (NIK kinase) signaling mediate the response in HSN. Although the AVM axon also migrates through this matrix, the mutations have little effect on the direction of AVM axon outgrowth, indicating that responses to the matrix are cell-specific. Together, these results suggest that an extracellular matrix can regulate the direction of UNC-6 guidance by increasing the probability that UNC-40-mediated axon outgrowth activity will be oriented in a specific direction.
The thermal phase behaviour of cryomilled a 0 -AlD 3 and a-AlD 3 was investigated by in situ synchrotron powder X-ray diffraction (SR-PXD), differential scanning calorimetry and first principles atomic modelling. In situ measurements showed that a 0 -AlD 3 decomposes directly into Al and D 2 at around 80 C during heating at 1 C min À1 . At higher temperatures the transformation of a 0 -AlD 3 to a-AlD 3 was observed by DSC measurements at 5 C min À1 , and tentatively by in situ SR-PXD at 1 C min À1 . Atomic modelling was carried out to investigate possible structural relationships and transformation pathways between the aand a 0 -phase. Group-subgroup relation analyses and direct method lattice dynamics were used to rule out a possible displacive transformation pathway between the a 0 -and a-phases. The likelihood of a reconstructive transformation was demonstrated by partial transformation of an interface between a 0 and a domains during elevated temperature molecular dynamics. Such an a 0 -to a-phase transformation may be possible when kinetic barriers can be overcome at elevated temperatures or during long time periods. These insights are also relevant to the transformation mechanisms of the b-AlD 3 and g-AlD 3 isomorphs to the a-phase.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.