A review on electrocatalytic CO_(2) conversion via C-C and C-N coupling

Electrochemical C-C and C-N coupling reactions with the conversion of abundant and inexpensive small molecules,such as CO_(2) and nitrogencontaining species,are considered a promising route for increasing the value of CO_(2) reduction products.The development of high-performance catalysts is the key to the both electrocatalytic reactions.In this review,we present a systematic summary of the reaction systems for electrocatalytic CO_(2) reduction,along with the coupling mechanisms of C-C and C-N bonds over outstanding electrocatalytic materials recently developed.The key intermediate species and reaction pathways related to the coupling as well as the catalyst-structure relationship will be also discussed,aiming to provide insights and guidance for designing efficient CO_(2) reduction systems.

BMP7 expression in mammalian cortical radial glial cells increases the length of the neurogenic period

The seat of human intelligence is the human cerebral cortex,which is responsible for our exceptional cognitive abilities.Identifying principles that lead to the development of the large-sized human cerebral cortex will shed light on what makes the human brain and species so special.The remarkable increase in the number of human cortical pyramidal neurons and the size of the human cerebral cortex is mainly because human cortical radial glial cells,primary neural stem cells in the cortex,generate cortical pyramidal neurons for more than 130 days,whereas the same process takes only about 7 days in mice.The molecular mechanisms underlying this difference are largely unknown.Here,we found that bone morphogenic protein 7(BMP7)is expressed by increasing the number of corti-cal radial glial cells during mammalian evolution(mouse,ferret,monkey,and human).BMP7 expression in cortical radial glial cells promotes neurogenesis,inhibits gliogenesis,and thereby increases the length of the neurogenic period,whereas Sonic Hedgehog(SHH)signaling promotes cortical gliogenesis.We demonstrate that BMP7 sign-aling and SHH signaling mutually inhibit each other through regulation of GLI3 repressor formation.We propose that BMP7 drives the evolutionary expansion of the mammalian cortex by increasing the length of the neurogenic period.

Decoding Cortical Glial Cell Development

Mouse cortical radial glial cells(RGCs)are primary neural stem cells that give rise to cortical oligodendrocytes,astrocytes,and olfactory bulb(OB)GABAergic interneurons in late embryogenesis.There are fundamental gaps in understanding how these diverse cell subtypes are generated.Here,by combining single-cell RNA-Seq with intersectional lineage analyses,we show that beginning at around E16.5,neocortical RGCs start to generate ASCL1^(+)EGFR^(+)apical multipotent intermediate progenitors(MIPCs),which then differentiate into basal MIPCs that express ASCL1,EGFR,OLIG2,and MKI67.These basal MIPCs undergo several rounds of divisions to generate most of the cortical oligodendrocytes and astrocytes and a subpopulation of OB interneurons.Finally,single-cell ATAC-Seq supported our model for the genetic logic underlying the specification and differentiation of cortical glial cells and OB interneurons.Taken together,this work reveals the process of cortical radial glial cell lineage progression and the developmental origins of cortical astrocytes and oligodendrocytes.

Homeobox Gene Six3 is Required for the Differentiation of D2-Type Medium Spiny Neurons

Medium spiny neurons(MSNs)in the striatum,which can be divided into D1 and D2 MSNs,originate from the lateral ganglionic eminence(LGE).Previously,we reported that Six3 is a downstream target of Sp8/Sp9 in the transcriptional regulatory cascade of D2 MSN development and that conditionally knocking out Six3 leads to a severe loss of D2 MSNs.Here,we showed that Six3 mainly functions in D2 MSN precursor cells and gradually loses its function as D2 MSNs mature.Conditional deletion of Six3 had little effect on cell proliferation but blocked the differentiation of D2 MSN precursor cells.In addition,conditional overexpression of Six3 promoted the differentiation of precursor cells in the LGE.We measured an increase of apoptosis in the postnatal striatum of conditional Six3-knockout mice.This suggests that,in the absence of Six3,abnormally differentiated D2 MSNs are eliminated by programmed cell death.These results further identify Six3 as an important regulatory element during D2 MSN differentiation.