Ageing populations pose one of the main public health crises of our time. Reprogramming gene expression by altering the activities of sequence-specific transcription factors (TFs) can ameliorate deleterious effects of age. Here we explore how a circuit of TFs coordinates pro-longevity transcriptional outcomes, which reveals a multi-tissue and multi-species role for an entire protein family: the E-twenty-six (ETS) TFs. In
Drosophila
, reduced insulin/IGF signalling (IIS) extends lifespan by coordinating activation of
Aop
, an ETS transcriptional repressor, and
Foxo
, a Forkhead transcriptional activator.
Aop
and
Foxo
bind the same genomic loci, and we show that, individually, they effect similar transcriptional programmes
in vivo
. In combination,
Aop
can both moderate or synergise with
Foxo
, dependent on promoter context. Moreover,
Foxo
and
Aop
oppose the gene-regulatory activity of
Pnt
, an ETS transcriptional activator. Directly knocking down
Pnt
recapitulates aspects of the
Aop
/
Foxo
transcriptional programme and is sufficient to extend lifespan. The lifespan-limiting role of
Pnt
appears to be balanced by a requirement for metabolic regulation in young flies, in which the
Aop-Pnt-Foxo
circuit determines expression of metabolic genes, and
Pnt
regulates lipolysis and responses to nutrient stress. Molecular functions are often conserved amongst ETS TFs, prompting us to examine whether other
Drosophila
ETS-coding genes may also affect ageing. We show that five out of eight Drosophila ETS TFs play a role in fly ageing, acting from a range of organs and cells including the intestine, adipose and neurons. We expand the repertoire of lifespan-limiting ETS TFs in
C
.
elegans
, confirming their conserved function in ageing and revealing that the roles of ETS TFs in physiology and lifespan are conserved throughout the family, both within and between species.
Employing channel adaptive resource allocation can yield to a large enhancement in almost any performance metric of Device-to-Device (D2D) communications. We observe that D2D users are able to estimate their local Channel State Information (CSI), however the base station needs some signaling exchange to acquire this information. Based on the D2D users' knowledge of their local CSI, we provide a scheduling framework that shows how distributed approach outperforms centralized one. We start by proposing a centralized scheduling that requires the knowledge of D2D links' CSI at the base station level. This CSI reporting suffers from the limited number of resources available for feedback transmission. Therefore, we benefit from the users' knowledge of their local CSI to develop a distributed algorithm for D2D resource allocation. In distributed approach, collisions may occur between the different CSI reporting; thus a collision reduction algorithm is proposed. We give a description on how both centralized and distributed algorithms can be implemented in practice. Furthermore, numerical results are presented to corroborate our claims and demonstrate the gain that the proposed scheduling algorithms bring to cellular networks.
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