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Research article2014Peer reviewedOpen access

A Tree Ortholog of APETALA1 Mediates Photoperiodic Control of Seasonal Growth

Azeez, Abdul; Miskolczi, Pal Csaba; Szymon, Tylewicz; Bhalerao, Rupali R.

Abstract

Background: Photoperiodic control of development plays a key role in adaptation of plants to seasonal changes. A signaling module consisting of CONSTANS (CO) and FLOWERING LOCUS T (FT) mediates in photoperiodic control of a variety of developmental transitions (e. g., flowering, tuberization, and seasonal growth cessation in trees). How this conserved CO/FT module can mediate in the photoperiodic control of diverse unrelated developmental programs is poorly understood.Results: We show that Like-AP1 (LAP1), a tree ortholog of Arabidopsis floral meristem identity gene APETALA1 (AP1), mediates in photoperiodic control of seasonal growth cessation downstream of the CO/FT module in hybrid aspen. Using LAP1 overexpressors and RNAi-suppressed transgenic trees, we demonstrate that short day (SD)-mediated downregulation of LAP1 expression is required for growth cessation. In contrast with AP1 targets in flowering, LAP1 acts on AINTEGUMENTA-like 1 transcription factor, which is implicated in SD-mediated growth cessation. Intriguingly, unlike AP1 in Arabidopsis, ectopic expression of LAP1 fails to induce early flowering in hybrid aspen trees.Conclusions: These results indicate that AP1 ortholog in trees has acquired a novel function in photoperiodic regulation of seasonal growth. Thus, photoperiodic signaling pathway may have diverged downstream of AP1/LAP1 rather than the CO/FT module during evolution. Moreover, control of flowering by the CO/FT module can be uncoupled from its role in photoperiodic control of seasonal growth in trees. Thus, our findings can explain mechanistically how a conserved signaling module can mediate in the control of a highly diverse set of developmental transitions by a similar input signal, namely photoperiod.

Published in

Current Biology
2014, Volume: 24, number: 7, pages: 717-724
Publisher: CELL PRESS