The phrase "activating origins" is correct and usable in written English.
It can be used in contexts related to initiating or bringing to life foundational elements or sources, possibly in discussions about technology, philosophy, or creative processes.
Example: "The project focuses on activating origins to inspire innovative solutions that draw from historical practices."
Alternatives: "initiating sources" or "engaging foundations".
In L. kluyveri, replication timing along chromosomes alternates between regions of early and late activating origins, except for the 1 Mb GC-rich chromosomal arm.
In addition, we showed that replication timing along chromosomes alternates between large regions of early and late activating origins as in S. cerevisiae (Raghuraman et al. 2001; Yabuki et al. 2002; Alvino et al. 2007; McCune et al. 2008).
In the genome, URA3 is flanked by two efficient early activating origins, ARS508 and ARS510, that are located at respective distances of 21.9 and 28.8 kb from URA3 (Nieduszynski et al. 2007).
S phase was significantly extended in all mutants, but the genome-wide replication program was hardly altered: the identity of activated origins and their relative activation times (or efficiencies) remained essentially the same as those in wild-type.
These findings support a model in which replication timing is the result of competing signals, which may determine the availability of replication factors to activate origins.
These include a local replication enhancer that activates origin firing at DAFC-66D (Orr-Weaver et al. 1989), ORC-independent origin firing at DAFC-34B (Kim and Orr-Weaver 2011), and local repression of ORC binding and origin activity at DAFC-22B (Kim et al. 2011).
Those licensed sites that do not activate (dormant origins) are passively replicated and are potential backup origins, available to rescue replication if forks stall irreversibly (Blow et al., 2011; Newman et al., 2013).
The simplest explanation for such a tendency would be that K36me1 helps to activate replication origins, but its effect can be counteracted by K36me3.
This simple system obviates the need for additional regulatory pathways to activate dormant origins when the cell undergoes replication stress.
However, CFS are unable to compensate for replication stress, and the inability to activate additional origins may impede the completion of replication leading to CFS destabilization.
The possible involvement of the replication checkpoint in the scaling phenotype was suggested [ 18, 19, 22], since deletion of either mec1 or rad53 activated late origins that were inhibited by HU treatment [ 23– 26].
