
KLF7 is a crucial factor for inducing human pluripotency, promoting reprogramming and boosting efficiency in chemical resetting to a naive state.


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Pluripotency is the capacity to give rise to all differentiated cells of the body and the germ line and is governed by a self-reinforcing network of transcription factors. The forced expression of only some of these factors enables the reprogramming of somatic cells to pluripotency. In murine cells, several kruppel-like factors (KLFs) have been identified as stabilisers and inducers of pluripotency. Human somatic cells are routinely reprogrammed by expression of KLF4 in combination with OCT4, SOX2 and cMYC (OSKM). An extensive transcriptome analysis revealed, however, that KLF4 is barely expressed in conventional human pluripotent stem cells (PSCs). Here we show that KLF7 is robustly expressed in conventional human PSCs and it allows transcription factor-mediated somatic reprogramming. Moreover, we find that KLF7 is highly expressed in naive PSCs and its forced expression in conventional hPSCs induces upregulation of naive markers and boosts efficiency of chemical resetting to naive PSCs, overall suggesting that KLF7 is a general human pluripotency factor and an inducer of pluripotency.

### Competing Interest Statement

The authors have declared no competing interest.

KLF7 is a general inducer of human pluripotency

klf7-key-inducer-of-human-pluripotency


KLF7: Key Inducer of Human Pluripotency


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Heterotypic interaction with osteoblasts promotes asymmetric division of human hematopoietic stem and progenitor cells.


Hematopoietic Stem and Progenitor Cells (HSPCs) give rise to all cell types of the hematopoietic system through various processes including asymmetric divisions. However, the contribution of stromal cells of the hematopoietic niches in the control of HSPC asymmetric divisions remains unknown. Using polyacrylamide microwells as minimalist niches, we show that heterotypic interaction with osteoblast promotes asymmetric division of human HSPC. Upon interaction, HSPCs polarize in interphase with centrosome, the Golgi apparatus and lysosomes positioned close to the site of contact. Subsequently during mitosis, HSPCs orient their spindle perpendicular to the plane of contact. This division gives rise to siblings with unequal amounts of lysosomes and differentiation markers such as CD34. Such asymmetric inheritance generates heterogeneity in the progeny, which is likely to be a key contributor to the plasticity of the early steps of hematopoiesis.

### Competing Interest Statement

The authors have declared no competing interest.

Heterotypic interaction promotes asymmetric division of human hematopoietic stem and progenitor cells

heterotypic-interaction-impact-on-human-hspc-asymmetric-division


Heterotypic Interaction Impact on Human HSPC Asymmetric Division
