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The VCAM1–ApoE pathway directs microglial chemotaxis and alleviates Alzheimer’s disease pathology

ABSTRACT: The VCAM1–ApoE pathway directs microglial chemotaxis and alleviates Alzheimer’s disease pathology

PROVIDER: PRJNA858001 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20097006_1.fastq.gz	Fastqsanger.gz
	SRR20097006_2.fastq.gz	Fastqsanger.gz
	SRR20097007_1.fastq.gz	Fastqsanger.gz
	SRR20097007_2.fastq.gz	Fastqsanger.gz
	SRR20097008_1.fastq.gz	Fastqsanger.gz

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Project description:Chemotaxis is used by free-living motile bacteria to swim towards nutrient sources or away from repellents, and to navigate the environment to locate niches optimal for growth and survival. Multiple chemotaxis systems have been identified in different bacterial species, including Azospirillum brasilense. In A. brasilense, chemotaxis is mediated by two distinct chemotaxis pathways, named Che1 and Che4, that physically interact to form mixed chemotaxis signaling arrays. Signaling from the Che1 and Che4 pathways control transient increases in swimming speed and swimming reversals, respectively, during chemotaxis. In A. brasilense, chemotaxis is tightly linked to energy metabolism with this coupling occurring through the sensory input of several energy-sensing chemoreceptors and through the control of chemoreceptor activity by the c-di-GMP second messenger. Previous work has demonstrated that chemotaxis in A. brasilense also affects unrelated cellular functions including cell-to-cell clumping and flocculation. However, the molecular mechanism for these effects is not known. Here, we identify additional effects of mutations abolishing Che1 (cheA1 mutant), Che4 (cheA4 mutant) or both Che1 and Che4 (cheA1/cheA4 mutant) function on nitrogen and carbon metabolism and use whole cell proteome and metabolome mass spectrometry to further characterize the interplay between chemotaxis and metabolism. We found that CheA1 mediates most changes in chemoreceptor arrays composition and also affects small molecules signaling while a mutant lacking CheA4 displays changes in nitrogen metabolism, including nitrate assimilation and nitrogen fixation. In contrast, the mutant lacking both CheA1 and CheA4, which lacks chemotaxis and does not form chemotaxis signaling arrays, displays distinct and non-overlapping changes that suggest the assembly of chemotaxis signaling arrays modulates energy and carbon metabolism. Together, the results suggest distinct roles for CheA1, CheA4 and chemotaxis signaling arrays in modulating chemotaxis and metabolism, likely through control of distinct global regulatory networks.

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The VCAM1–ApoE pathway directs microglial chemotaxis and alleviates Alzheimer’s disease pathology

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