MYB28 (At5g61420; HAG1/PMG1) - manual literature synthesis

No deep-research API was available for this review; this summary was compiled by hand from the
cached publications in publications/ and the UniProt record Q9SPG2. All quotes are verbatim
from the cited source.

Identity

• UniProt Q9SPG2 (MYB28_ARATH), TAIR AT5G61420, GeneID 836263; 366 aa R2R3-MYB transcription
  factor (two Myb_DNA-binding Pfam domains, PF00249; InterPro IPR015495 Myb_TF_plants).
  Synonyms HAG1 (HIGH ALIPHATIC GLUCOSINOLATE 1) and PMG1 (PRODUCTION OF METHIONINE-DERIVED
  GLUCOSINOLATE 1). Subgroup 12 R2R3-MYB with MYB29/HAG3, MYB76/HAG2 (aliphatic) and
  MYB34/MYB51/MYB122 (indolic).

Function: master positive regulator of aliphatic glucosinolate biosynthesis

• Identified in a transactivation screen: "In a screen for the trans-activation potential of
  various transcription factors toward glucosinolate biosynthetic genes, we could identify the
  HAG1 (HIGH ALIPHATIC GLUCOSINOLATE 1, also referred to as MYB28) gene as a positive regulator of
  aliphatic methionine-derived glucosinolates" PMID:17521412.
• Co-expression / omics, knockout and overexpression: "PMG1/Myb28 is apparently a master
  transcription factor, generally regulating the pathway from Met to aliphatic GSLs, and is
  necessary and sufficient for the biosynthesis of aliphatic GSLs at a basal level in
  Arabidopsis" PMID:17420480. In myb28 "the expression of most of the genes involved in
  aliphatic GSL biosynthesis was repressed" PMID:17420480; overexpression in suspension cells
  activated every aliphatic GSL structural gene and produced GSLs in dedifferentiated cells
  PMID:17420480.
• Redundancy with MYB29: "in the absence of both, the synthesis of all aliphatic glucosinolates
  is blocked" PMID:18446225; myb28 blocks long-chain aliphatic GSLs PMID:18446225.
• Reciprocal transactivation among HAG1/MYB28, HAG2/MYB76, HAG3/MYB29 and repression of indolic
  GSL regulators PMID:18042203. Complementation of myb28myb29 with pMYB28:MYB28 "activated AGSL
  biosynthetic genes and restored accumulation of AGSLs with short side chains" PMID:23792303.
• Network view: MYB28/MYB29/MYB76 interplay determines aliphatic GSL profile; chemotype partly
  uncoupled from biosynthetic transcript levels PMID:20348214.
• Direct promoter binding: in a large Y1H screen MYB28 "has been validated to interact with
  these promoters" of aliphatic GSL genes PMID:25352272; additional Y1H network screens
  (secondary cell wall, nitrogen metabolism) also recorded MYB28 promoter interactions
  [PMID:25533953, PMID:30356219] (supplementary data, not inspected here).
• Partners: MYC2/MYC3/MYC4 bHLH factors "interact directly with GS-related MYBs" (Y2H and
  pull-down) PMID:23943862; UniProt: "Can form complexes with MYC2, MYC3 or MYC4."
• Brassinosteroid repression of GSLs requires MYB28 PMID:23580754.

Location and expression

• Nucleus (UniProt; ECO:0000269 PubMed:17521412; PROSITE-ProRule PRU00625).
• Expressed in generative organs, mature leaves and trichomes; induced by touch/wounding in
  inflorescences, by glucose [PMID:17521412, PMID:23115560].
• Sulfur: Hirai et al. report MYB28 down-regulated under sulfur deficiency PMID:17420480,
  whereas Li et al. report MYB28 "expression was induced by sulfur deficiency" PMID:23792303
• conflicting reports on direction.
• Herbivory/biotic: aphid feeding down-regulated MYB28/29/76 transcripts PMID:23144921;
  lepidopteran oral secretions suppress basal MYB28 expression PMID:40546745.

Physiological consequences (indirect, via glucosinolates)

• Overexpression reduced weight gain of Spodoptera exigua PMID:17521412; myb28myb29 increases
  Mamestra brassicae larval weight gain PMID:18446225.
• myb28 hypersusceptible to Sclerotinia sclerotiorum PMID:21418358.
• myb28myb29 lost Pseudomonas fluorescens SS101-induced resistance to Pst PMID:23073694.