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See detailColor Vision: Decoding Color Space
Retter, Talia UL; Webster, Michael A.

in Current Biology (2021), 31(3), 122-124

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See detailExogenous covert shift of attention without the ability to plan eye movements.
Masson, Nicolas UL; Andres, Michael; Pereira, Sarah Carneiro et al

in Current Biology (2020), 30(18), 1032-1033

The automatic allocation of attention to a salient stimulus in the visual periphery (e.g., a traffic light turning red) while maintaining fixation elsewhere (e.g., on the car ahead) is referred to as ... [more ▼]

The automatic allocation of attention to a salient stimulus in the visual periphery (e.g., a traffic light turning red) while maintaining fixation elsewhere (e.g., on the car ahead) is referred to as exogenous covert shift of attention (ECSA). An influential explanation is that ECSA results from the programming of a saccadic eye movement toward the stimulus of interest [1,2], although the actual movement may be withheld if needed. In this paper, however, we report evidence of ECSA in the paralyzed axis of three individuals with either horizontal or vertical congenital gaze paralysis, including for stimuli appearing at locations that cannot be foveated through head movements. This demonstrates that ECSA does not require programming either eye or head movements and calls for a re-examination of the oculomotor account. [less ▲]

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See detailEvolutionary Genomics and Conservation of the Endangered Przewalski's Horse.
Der Sarkissian, Clio; Ermini, Luca; Schubert, Mikkel et al

in Current Biology (2015), 25(19), 2577-83

Przewalski's horses (PHs, Equus ferus ssp. przewalskii) were discovered in the Asian steppes in the 1870s and represent the last remaining true wild horses. PHs became extinct in the wild in the 1960s but ... [more ▼]

Przewalski's horses (PHs, Equus ferus ssp. przewalskii) were discovered in the Asian steppes in the 1870s and represent the last remaining true wild horses. PHs became extinct in the wild in the 1960s but survived in captivity, thanks to major conservation efforts. The current population is still endangered, with just 2,109 individuals, one-quarter of which are in Chinese and Mongolian reintroduction reserves [1]. These horses descend from a founding population of 12 wild-caught PHs and possibly up to four domesticated individuals [2-4]. With a stocky build, an erect mane, and stripped and short legs, they are phenotypically and behaviorally distinct from domesticated horses (DHs, Equus caballus). Here, we sequenced the complete genomes of 11 PHs, representing all founding lineages, and five historical specimens dated to 1878-1929 CE, including the Holotype. These were compared to the hitherto-most-extensive genome dataset characterized for horses, comprising 21 new genomes. We found that loci showing the most genetic differentiation with DHs were enriched in genes involved in metabolism, cardiac disorders, muscle contraction, reproduction, behavior, and signaling pathways. We also show that DH and PH populations split approximately 45,000 years ago and have remained connected by gene-flow thereafter. Finally, we monitor the genomic impact of approximately 110 years of captivity, revealing reduced heterozygosity, increased inbreeding, and variable introgression of domestic alleles, ranging from non-detectable to as much as 31.1%. This, together with the identification of ancestry informative markers and corrections to the International Studbook, establishes a framework for evaluating the persistence of genetic variation in future reintroduced populations. [less ▲]

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See detailRetromer Binding to FAM21 and the WASH Complex Is Perturbed by the Parkinson Disease-Linked VPS35(D620N) Mutation.
McGough, Ian J.; Steinberg, Florian; Jia, Da et al

in Current Biology (2014)

Retromer is a protein assembly that plays a central role in orchestrating export of transmembrane-spanning cargo proteins from endosomes into retrieval pathways destined for the Golgi apparatus and the ... [more ▼]

Retromer is a protein assembly that plays a central role in orchestrating export of transmembrane-spanning cargo proteins from endosomes into retrieval pathways destined for the Golgi apparatus and the plasma membrane [1]. Recently, a specific mutation in the retromer component VPS35, VPS35(D620N), has linked retromer dysfunction to familial autosomal dominant and sporadic Parkinson disease [2, 3]. However, the effect of this mutation on retromer function remains poorly characterized. Here we established that in cells expressing VPS35(D620N) there is a perturbation in endosome-to-TGN transport but not endosome-to-plasma membrane recycling, which we confirm in patient cells harboring the VPS35(D620N) mutation. Through comparative stable isotope labeling by amino acids in cell culture (SILAC)-based analysis of wild-type VPS35 versus the VPS35(D620N) mutant interactomes, we establish that the major defect of the D620N mutation lies in the association to the actin-nucleating Wiskott-Aldrich syndrome and SCAR homolog (WASH) complex. Moreover, using isothermal calorimetry, we establish that the primary defect of the VPS35(D620N) mutant is a 2.2 +/- 0.5-fold decrease in affinity for the WASH complex component FAM21. These data define the primary molecular defect in retromer assembly that arises from the VPS35(D620N) mutation and, by revealing functional effects on retromer-mediated endosome-to-TGN transport, provide new insight into retromer deregulation in Parkinson disease. [less ▲]

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See detailCHD4 Is a RanGTP-Dependent MAP that Stabilizes Microtubules and Regulates Bipolar Spindle Formation
Koffa, Maria UL; Yokoyama, Hideki; Nakos, Konstantinos et al

in Current Biology (2013), 23(24), 2443-2451

Background Production of the GTP-bound form of the Ran GTPase (RanGTP) around chromosomes induces spindle assembly by activating nuclear localization signal (NLS)-containing proteins. Several NLS proteins ... [more ▼]

Background Production of the GTP-bound form of the Ran GTPase (RanGTP) around chromosomes induces spindle assembly by activating nuclear localization signal (NLS)-containing proteins. Several NLS proteins have been identified as spindle assembly factors, but the complexity of the process led us to search for additional proteins with distinct roles in spindle assembly. Results We identify a chromatin-remodeling ATPase, CHD4, as a RanGTP-dependent microtubule (MT)-associated protein (MAP). MT binding occurs via the region containing an NLS and chromatin-binding domains. In Xenopus egg extracts and cultured cells, CHD4 largely dissociates from mitotic chromosomes and partially localizes to the spindle. Immunodepletion of CHD4 from egg extracts significantly reduces the quantity of MTs produced around chromatin and prevents spindle assembly. CHD4 RNAi in both HeLa and Drosophila S2 cells induces defects in spindle assembly and chromosome alignment in early mitosis, leading to chromosome missegregation. Further analysis in egg extracts and in HeLa cells reveals that CHD4 is a RanGTP-dependent MT stabilizer. Moreover, the CHD4-containing NuRD complex promotes organization of MTs into bipolar spindles in egg extracts. Importantly, this function of CHD4 is independent of chromatin remodeling. Conclusions Our results uncover a new role for CHD4 as a MAP required for MT stabilization and involved in generating spindle bipolarity. © 2013 Elsevier Ltd. [less ▲]

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See detailBrain plasticity: Paradoxical case of a neurodegenerative disease?
Cardoso-Leite, Pedro UL; Ascher, Philippe; Bavelier, Daphne

in Current Biology (2012), 22(20), 884-6

A thought-provoking new study has found that symptom-free carriers of the neurodegenerative Huntington's disease present a dramatic two-fold acceleration in perceptual learning.

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See detailSTAT5 contributes to interferon resistance of melanoma cells
Wellbrock, C.; Weisser, C.; Hassel, J. C. et al

in Current Biology (2005), 15(18), 1629-39

BACKGROUND: Malignant melanoma is a highly aggressive neoplastic disease whose incidence is increasing rapidly. In recent years, the use of interferon alpha (IFNalpha) has become the most established ... [more ▼]

BACKGROUND: Malignant melanoma is a highly aggressive neoplastic disease whose incidence is increasing rapidly. In recent years, the use of interferon alpha (IFNalpha) has become the most established adjuvant immunotherapy for melanoma of advanced stage. IFNalpha is a potent inhibitor of melanoma cell proliferation, and the signal transducer and activator of transcription STAT1 is crucial for its antiproliferative action. Although advanced melanomas clinically resistant to IFNalpha are frequently characterized by inefficient STAT1 signaling, the mechanisms underlying advanced-stage interferon resistance are poorly understood. RESULTS: Here, we demonstrate that IFNalpha activates STAT5 in melanoma cells and that in IFNalpha-resistant cells STAT5 is overexpressed. Significantly, the knockdown of STAT5 in interferon-resistant melanoma cells restored the growth-inhibitory response to IFNalpha. When STAT5 was overexpressed in IFNalpha-sensitive cells, it counteracted interferon-induced growth inhibition. The overexpressed STAT5 diminished IFNalpha-triggered STAT1 activation, most evidently through upregulation of the inhibitor of cytokine-signaling CIS. CONCLUSIONS: Our data demonstrate that overexpression and activation of STAT5 enable melanoma cells to overcome cytokine-mediated antiproliferative signaling. Thus, overexpression of STAT5 can counteract IFNalpha signaling in melanoma cells, and this finally can result in cytokine-resistant and progressively growing tumor cells. These findings have significant implications for the clinical failure of IFNalpha therapy of advanced melanoma because they demonstrate that IFNalpha induces the activation of STAT5 in melanoma cells, and in STAT5-overexpressing cells, this contributes to IFNalpha resistance. [less ▲]

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