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Forebrain Eml1 depletion reveals early centrosomal dysfunction causing subcortical heterotopia

ABSTRACT: The layered structure of the cerebral cortex is formed through a complicated sequence of highly controlled stages during corticogenesis. The perturbation of neuronal migration and cell division during this process can result a rare disorder called as cortical heterotopia. EML1 is a heterotopia associated gene where the perturbations cause heterotopia formation in human as well as in mouse. To elaborate on the EML1 interactome and its disruptions by heterotopia-associated mutation, we performed BioID proximity labeling of EML1 and EML1*T243A, a human SH-associated mutant form of the protein.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Neuro-2a Cell

SUBMITTER: Berfu Nur Yiğit

LAB HEAD: Prof. Dr.

PROVIDER: PXD045846 | Pride | 2024-08-26

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	20200817_BioID_Firstset_NT.msf	Msf
	20200817_BioID_Firstset_NT.raw	Raw
	20200817_BioID_Firstset_N_EML1.msf	Msf
	20200817_BioID_Firstset_N_EML1.raw	Raw
	20200817_BioID_Firstset_N_EML1_T243A.msf	Msf

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Project description:The cerebral cortex is a highly organized structure whose development depends on different progenitor cell types. These give rise to post-mitotic neurons that migrate across the developing cortical wall to their final positions in the cortical plate. Apical radial glia cells (aRGs) are the main progenitor type in early corticogenesis, responsible for the production of other progenitors, and regulating the final neuronal output. Abnormal behavior of aRG can severely impact corticogenesis resulting in cortical malformations. Mutations in the microtubule associated protein Eml1 lead to severe subcortical heterotopia, characterized by the presence of aberrantly located neurons beneath the normotopic cortex. Mutations in EML1/Eml1 have been reported in three families presenting severe atypical heterotopia, as well as in the Heterotopic cortex ‘HeCo’ spontaneous mouse mutant. In the latter, ectopically cycling aRGs were found cycling outside their normal proliferative ventricular zone (VZ) from early stages of corticogenesis (Croquelois et al., 2009, Kielar et al., 2014, Shaheen et al., 2017). Ectopic aRGs are likely to be responsible for the formation of the heterotopia. It is thus crucial to understand the role of Eml1 in aRGs to elucidate the physiological and pathological mechanisms causing aRGs to leave the VZ. The role of Eml1 in aRGs remains vastly unexplored. We have thus performed mass spectrometry with embryonic cortex lysates (E13.5) to shed light on the intracellular pathways and molecular mechanisms in which Eml1 could be involved. This data combined with other cell biology and biochemistry approaches will contribute to understand the role of this heterotopia protein at early stages of development.

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