SUPPRESSOR OF MORE AXILLARY GROWTH2 1 controls seed germination and seedling development in Arabidopsis

Abiotic chemical signals discovered in smoke that are known as karrikins (KARs) and the endogenous hormone strigolactone (SL) control plant growth through a shared <i>MORE AXILLARY GROWTH2 (MAX2)</i>-dependent pathway. A SL biosynthetic pathway and candidate KAR/SL receptors have been characterized, but signaling downstream of MAX2 is poorly defined. A screen for genetic suppressors of the enhanced seed dormancy phenotype of <i>max2</i> in Arabidopsis (<i>Arabidopsis thaliana</i>) led to identification of a <i>suppressor of max2 1 (smax1)</i> mutant. <i>smax1</i> restores the seed germination and seedling photomorphogenesis phenotypes of <i>max2</i> but does not affect the lateral root formation, axillary shoot growth, or senescence phenotypes of <i>max2</i>. Expression of three transcriptional markers of KAR/SL signaling, <i>D14-LIKE2, KAR-UP F-BOX1</i>, and <i>INDOLE-3-ACETIC ACID INDUCIBLE1</i>, is rescued in <i>smax1 max2</i> seedlings. <i>SMAX1</i> is a member of an eight-gene family in Arabidopsis that has weak similarity to <i>HEAT SHOCK PROTEIN 101</i>, which encodes a caseinolytic peptidase B chaperonin required for thermotolerance. <i>SMAX1</i> and the <i>SMAX1-like (SMXL)</i> homologs are differentially expressed in Arabidopsis tissues. <i>SMAX1</i> transcripts are most abundant in dry seed, consistent with its function in seed germination control. Several <i>SMXL</i> genes are up-regulated in seedlings treated with the synthetic SL GR24. <i>SMAX1</i> and <i>SMXL2</i> transcripts are reduced in <i>max2</i> seedlings, which could indicate negative feedback regulation by KAR/SL signaling. <i>smax1</i> seed and seedling growth mimics the wild type treated with KAR/SL, but <i>smax1</i> seedlings are still responsive to 2<i>H</i>-furo[2,3-<i>c</i>]pyran-2-one (KAR₂) or GR24. We conclude that SMAX1 is an important component of KAR/SL signaling during seed germination and seedling growth but is not necessary for all MAX2-dependent responses. We hypothesize that one or more SMXL proteins may also act downstream of MAX2 to control the diverse developmental responses to KARs and SLs.