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Corticothalamic interactions between associative cortices and higher order thalamic nuclei are involved in high‐cognitive functions such as decision‐making and working memory. Corticothalamic neurons (CTn) in the prefrontal cortex and other associative areas have been much less studied than their counterparts in the primary sensory areas. The availability of characterized transgenic tools to study CTn in associative areas will facilitate their study and contribute to overcome the scarcity of data about their properties, network dynamics, and contribution to cognitive functions. Here, we characterized the Syt6‐Cre (KI148Gsat/Mmud) transgenic mouse line, by tracking expression of a Cre‐mediated reporter. In this line, Cre‐reporter is strongly expressed in the prefrontal, motor, cingulate, and retrosplenial cortices, as well as in other brain areas including the cerebellum and the olfactory tubercle. Cortical expression starts embryonically and reaches the adult expression pattern by postnatal day 15. In the cortex, Cre‐reporter is expressed by layer 6‐CTn and by layer 5‐CTn to a lesser extent. We quantified Syt6‐Cre+ CTn axon varicosities to estimate the distribution and density of putative corticothalamic driver and modulator inputs to thalamic nuclei in the medial, midline, intralaminar, anterior, and motor groups. Also, we characterized the effect of optogenetic stimulation of Syt6‐Cre+ neurons in the activity of the prefrontal cortex. CTn stimulation in the prefrontal cortex induces an oscillatory activity in the local field potential that resembles the cortical downstates typically observed during slow‐wave sleep or quiet wake. [ABSTRACT FROM AUTHOR]

New roles for RNA in mediating gene expression are being discovered at an alarming rate. A broad array of pathways control patterning of N6-methyladenosine (m6A) methylation on RNA transcripts. This review comprehensively discusses long non-coding RNAs (lncRNAs) as an additional dynamic regulator of m6A methylation, with a focus on the untranslated regions (UTRs) of mRNAs. Although there is extensive literature describing m6A modification of lncRNA, the function of lncRNA in guiding m6A writers has not been thoroughly explored. The independent control of lncRNA expression, its heterogeneous roles in RNA metabolism, and its interactions with epigenetic machinery, alludes to their potential in dynamic patterning of m6A methylation. While epigenetic regulation by histone modification of H3K36me3 has been demonstrated to pattern RNA m6A methylation, these modifications were specific to the coding and 3′UTR regions. However, there are observations that 5′UTR m6A is distinct from that of the coding and 3′UTR regions, and substantial evidence supports the active regulation of 5′UTR m6A methylation. Consequently , two potential mechanisms in patterning the UTRs m6A methylation are discussed; (1) Anti-sense lncRNA (AS-lncRNA) can either bind directly to the UTR, or (2) act indirectly via recruitment of chromatin-modifying complexes to pattern m6A. Both pathways can guide the m6A writer complex, facilitate m6A methylation and modulate protein translation. Findings in the lncRNA-histone-m6A axis could potentially contribute to the discovery of new functions of lncRNAs and clarify lncRNA-m6A findings in translational medicine. [ABSTRACT FROM AUTHOR]

New roles for RNA in mediating gene expression are being discovered at an alarming rate. A broad array of pathways control patterning of N 6 -methyladenosine (m 6 A) methylation on RNA transcripts. This review comprehensively discusses long non-coding RNAs (lncRNAs) as an additional dynamic regulator of m 6 A methylation, with a focus on the untranslated regions (UTRs) of mRNAs. Although there is extensive literature describing m 6 A modification of lncRNA, the function of lncRNA in guiding m 6 A writers has not been thoroughly explored. The independent control of lncRNA expression, its heterogeneous roles in RNA metabolism, and its interactions with epigenetic machinery, alludes to their potential in dynamic patterning of m 6 A methylation. While epigenetic regulation by histone modification of H3K36me3 has been demonstrated to pattern RNA m 6 A methylation, these modifications were specific to the coding and 3'UTR regions. However, there are observations that 5'UTR m 6 A is distinct from that of the coding and 3'UTR regions, and substantial evidence supports the active regulation of 5'UTR m 6 A methylation. Consequently , two potential mechanisms in patterning the UTRs m 6 A methylation are discussed; (1) Anti-sense lncRNA (AS-lncRNA) can either bind directly to the UTR, or (2) act indirectly via recruitment of chromatin-modifying complexes to pattern m 6 A. Both pathways can guide the m 6 A writer complex, facilitate m 6 A methylation and modulate protein translation. Findings in the lncRNA-histone-m 6 A axis could potentially contribute to the discovery of new functions of lncRNAs and clarify lncRNA-m 6 A findings in translational medicine., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Vaasjo.)