城市学校心理学家时间利用研究

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"时间利用研究:城市环境中学校心理学家的工作实况" 这篇学术论文"Time Utilization Study of School Psychologists in an Urban Setting"由Susan Brown Eitel、John J. Lambeth(来自新泽西州特伦顿公立学校)以及Irwin A. Hyman(来自天普大学)共同撰写。研究主要关注的是在一个中等规模的城市学区,通过时间抽样法来了解学校心理学家的实际工作角色和功能。研究人员训练了观察员记录心理学家的工作活动,以获取准确的数据。 研究表明,大约30-40%的心理学家工作时间用于评估任务,这一结果与自我报告的研究相吻合。尽管这些数据的普适性可能有限,但研究的主要目的是展示有效的研究方法,并作为进一步研究的启发式模型。在财政资源日益减少的时代,对于学校心理学家的角色定位问题,尤其是责任可追溯性的问题,这样的信息显得尤为重要。 随着PL94-142法案的实施,学校心理学家的评估角色被压缩,他们需要证明更广泛职能的合理性,这增加了获取此类信息的需求。许多研究集中在心理学家在不同功能上花费的时间比例,包括咨询、干预、教学支持以及其他与学生福祉相关的活动。然而,基于数据的信息仍然相对匮乏。 这项研究强调了时间利用分析在理解学校心理学家工作负载和职责分配方面的重要性,这对于政策制定者、教育管理者以及心理学家自身来说,都是规划工作、优化资源分配和提升服务效率的关键参考。此外,这样的研究也有助于推动学校心理学领域的发展,以便更好地满足学生和学校社区的需求。

Rab GTPases serve as master regulators of membrane trafficking. They can be activated by guanine nucleotide exchange factors (GEF) and be inactivated by GTPase-activating proteins (GAPs). The roles of some GAPs have been explored in Saccharomyces cerevisiae, but are largely unknown in filamentous fungi. Here, we investigated the role of GAP Gyp3 gene, an ortholog of S. cerevisiae Gyp3, in an entomopathogenic fungus, Metarhizium acridum. We found that MaGyp3 is mainly localized to the endoplasmic reticulum (ER) of vegetative hyphae, nuclei of mature conidia, and both ER and nuclei in invasive hyphae. Lack of MaGyp3 caused a decreased tolerance to hyperosmotic stress, heat-shock and UV-B radiation. Moreover, the ΔMaGyp3 mutant showed a significantly decreased pathogenicity owing to delayed germination, reduced appressorium-mediated penetration and impaired invasive growth. Loss of MaGyp3 also caused impaired fungal growth, advanced conidiation and defects in utilization of carbon and nitrogen sources, while overexpression of MaGyp3 exhibited delayed conidiation on nutrient-rich medium and conidiation pattern shift from microcycle conidiation to normal conidiation on nutrient-limited medium. Mavib-1, a tanscription factor invloved in conidiation by affecting nutrient utilizaiton, can directly bind to the promoter of MaGyp3. ΔMaGyp3 and ΔMavib-1 mutants shared similar phenotypes, and overexpression mutants of MaGyp3 and Mavib-1 (Mavib-1-OE) exhibited similar phenotypes in growth, conidiation and pathogenicity. Reintroduction of the Magyp3 driven by strong promoter gpd in ΔMavib-1 mutant recovered the defects in growth and conidiation for dysfunction of Mavib1. Taken together, our findings uncovered the role of GAP3 in a filamentous pathogenic fungus and and illustrated the upstream regulatory mechanism by direct interaction with Mavib-1.

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