Development of several epidermal cell types can be specified by the same MYB-related plant transcription factor

Development ◽  
1998 ◽  
Vol 125 (17) ◽  
pp. 3497-3508 ◽  
Author(s):  
B.J. Glover ◽  
M. Perez-Rodriguez ◽  
C. Martin

A MYB-related transcription factor (MIXTA) that controls development of conical cell form is expressed only in the inner epidermis of Antirrhinum petals. Expression of this gene throughout transgenic tobacco plants leads to excess numbers of multicellular trichomes on leaves and floral organs as well as the novel production of conical cells on leaves. These data indicate that conical cells and trichomes are produced by a common developmental pathway. The timing of MIXTA expression suggests that the choice between the cell types depends on the competence for cell division at the time at which the controlling gene is expressed. Duplication of genes and their association with different cis-regulatory regions may therefore result in the specification of novel plant cell types.

2018 ◽  
Author(s):  
Kimberley N. Babos ◽  
Kate E. Galloway ◽  
Kassandra Kisler ◽  
Madison Zitting ◽  
Yichen Li ◽  
...  

AbstractAlthough cellular reprogramming continues to generate new cell types, reprogramming remains a rare cellular event. The molecular mechanisms that limit reprogramming, particularly to somatic lineages, remain unclear. By examining fibroblast-to-motor neuron conversion, we identify a previously unappreciated dynamic between transcription and replication that determines reprogramming competency. Transcription factor overexpression forces most cells into states that are refractory to reprogramming and are characterized by either hypertranscription with little cell division, or hyperproliferation with low transcription. We identify genetic and chemical factors that dramatically increase the number of cells capable of both hypertranscription and hyperproliferation. Hypertranscribing, hyperproliferating cells reprogram at 100-fold higher, near-deterministic rates. We demonstrate that elevated topoisomerase expression endows cells with privileged reprogramming capacity, suggesting that biophysical constraints limit cellular reprogramming to rare events.


2017 ◽  
Vol 118 (11) ◽  
pp. 3662-3674 ◽  
Author(s):  
Oscar A. Vega ◽  
Claudia M.J. Lucero ◽  
Hector F. Araya ◽  
Sofia Jerez ◽  
Julio C. Tapia ◽  
...  

Author(s):  
Coenraad R. van Beek ◽  
Tapiwa Guzha ◽  
Nolusindiso Kopana ◽  
Cornelius S. van der Westhuizen ◽  
Sanjib K. Panda ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Dahai Wang ◽  
Nabil Rabhi ◽  
Shaw-Fang Yet ◽  
Stephen R. Farmer ◽  
Matthew D. Layne

AbstractThe vascular adventitia contains numerous cell types including fibroblasts, adipocytes, inflammatory cells, and progenitors embedded within a complex extracellular matrix (ECM) network. In response to vascular injury, adventitial progenitors and fibroblasts become activated and exhibit increased proliferative capacity and differentiate into contractile cells that remodel the ECM. These processes can lead to vascular fibrosis and disease progression. Our previous work established that the ECM protein aortic carboxypeptidase-like protein (ACLP) promotes fibrotic remodeling in the lung and is activated by vascular injury. It is currently unknown what controls vascular adventitial cell differentiation and if ACLP has a role in this process. Using purified mouse aortic adventitia Sca1+ progenitors, ACLP repressed stem cell markers (CD34, KLF4) and upregulated smooth muscle actin (SMA) and collagen I expression. ACLP enhanced myocardin-related transcription factor A (MRTFA) activity in adventitial cells by promoting MRTFA nuclear translocation. Sca1 cells from MRTFA-null mice exhibited reduced SMA and collagen expression induced by ACLP, indicating Sca1 cell differentiation is regulated in part by the ACLP-MRTFA axis. We determined that ACLP induced vessel contraction and increased adventitial collagen in an explant model. Collectively these studies identified ACLP as a mediator of adventitial cellular differentiation, which may result in pathological vessel remodeling.


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