TY - JOUR

T1 - A model for generating several adaptive phenotypes from a single genetic event

T2 - Saccharomyces cerevisiae GAP1 as a potential bet-hedging switch

AU - Møller, Henrik D

AU - Andersen, Kaj S

AU - Regenberg, Birgitte

PY - 2013

Y1 - 2013

N2 - Microbial populations adapt to environmental fluctuations through random switching of fitness-related traits in individual cells. This increases the likelihood that a subpopulation will be adaptive in a future milieu. However, populations are particularly challenged when several environment factors change simultaneously. We suggest that a population can rapidly adapt to multiple environmental changes if individual members stochastically flip a hub-switch that controls a set of adaptive phenotypes in a single event. This mechanism of coupling phenotypic outcomes via a hub-switch can protect a population against large fluctuations in size. Here we report that the general amino acid transporter Gap1 is a potential hub-switch. The GAP1 gene is flanked by two direct repeats that can lead to GAP1 deletions (∆gap1) and a self-replicating GAP1 circle. Thus, an isogenic GAP1 population can differentiate into two variant, reversible genotypes, ∆gap1 or GAP1 (circle). These subpopulations have different phenotypic advantages. A ∆gap1 population has a selective advantage on allantoin or ammonium as a nitrogen source and high stress tolerance. Advantages of the GAP1 population include amino acid uptake, fast energy recruitment by trehalose mobilization, and in some cases, adherent biofilm growth. Our proposed model of a hub-switch locus enhances the bet-hedging model of population dynamics.

AB - Microbial populations adapt to environmental fluctuations through random switching of fitness-related traits in individual cells. This increases the likelihood that a subpopulation will be adaptive in a future milieu. However, populations are particularly challenged when several environment factors change simultaneously. We suggest that a population can rapidly adapt to multiple environmental changes if individual members stochastically flip a hub-switch that controls a set of adaptive phenotypes in a single event. This mechanism of coupling phenotypic outcomes via a hub-switch can protect a population against large fluctuations in size. Here we report that the general amino acid transporter Gap1 is a potential hub-switch. The GAP1 gene is flanked by two direct repeats that can lead to GAP1 deletions (∆gap1) and a self-replicating GAP1 circle. Thus, an isogenic GAP1 population can differentiate into two variant, reversible genotypes, ∆gap1 or GAP1 (circle). These subpopulations have different phenotypic advantages. A ∆gap1 population has a selective advantage on allantoin or ammonium as a nitrogen source and high stress tolerance. Advantages of the GAP1 population include amino acid uptake, fast energy recruitment by trehalose mobilization, and in some cases, adherent biofilm growth. Our proposed model of a hub-switch locus enhances the bet-hedging model of population dynamics.

U2 - 10.4161/cib.23933

DO - 10.4161/cib.23933

M3 - Journal article

C2 - 23713139

VL - 6

SP - 1

EP - 4

JO - Communicative & Integrative Biology

JF - Communicative & Integrative Biology

SN - 1942-0889

IS - 3

M1 - e23933

ER -