In the notch signaling pathway, what is Fringe activating?
Usually, in such depictions where a species is pointing to a reaction or an interaction, the arrows mean that the species affects that reaction (for example, catalysis by an enzyme ). Generally pointy arrow heads denote positive effect (enhancing the reaction, for example an enzyme) and flat heads denote a negative interaction (repression). An arrow from one molecule to another can be used to depict a conversion (like glucose converting to glucose 6 phosphate). 

There are no real standards on how to depict a pathway. So, it can be confusing. 

In this case, Fringe actually alters Notch signalling (see below). So the arrow makes sense. However, the figure also has an arrow from Delta to Notch which can be interpreted as Delta getting converted to Notch. They also show an arrow from Notch to NICD which actually means a conversion. I would say that the depictions in this figure are inconsistent. 

From NCBI Gene entry on Human homolog of Fringe, LFNG:


  This gene is a member of the glycosyltransferase 31 gene family.
  Members of this gene family, which also includes the MFNG (GeneID:
  4242) and RFNG (GeneID: 5986) genes, encode evolutionarily conserved
  glycosyltransferases that act in the Notch signaling pathway to define
  boundaries during embryonic development. While their genomic structure
  is distinct from other glycosyltransferases, these proteins have a
  fucose-specific beta-1,3-N-acetylglucosaminyltransferase activity that
  leads to elongation of O-linked fucose residues on Notch, which alters
  Notch signaling. The protein encoded by this gene is predicted to be a
  single-pass type II Golgi membrane protein but it may also be secreted
  and proteolytically processed like the related proteins in mouse and
  Drosophila (PMID: 9187150). Mutations in this gene have been
  associated with autosomal recessive spondylocostal dysostosis 3.
  [provided by RefSeq, May 2018]


From Shao et al (2002):


  Recent studies have demonstrated that O-fucose modifications play an
  essential role in Notch function. Reduction of O-fucosyltransferase
  expression in Drosophila using RNAi (11) or in mice by gene ablation2
  causes Notch-like phenotypes, suggesting that O-fucose modifications
  are essential for Notch function. In addition, we and others have
  shown that Notch activation is modulated by extension of O-fucose on
  Notch with the fucose-specific β1,3-N-acetylglucosaminyltransferase
  Fringe (for recent reviews, see Refs. 12 and 13). Fringe was first
  identified in Drosophila and shown to inhibit Notch's ability to
  respond to Serrate but to potentiate its ability to respond to Delta
  (14). Three Drosophila Fringe homologues have been identified in
  mammals: Lunatic fringe (Lfng), Manic fringe (Mfng), and Radical
  fringe (Rfng) (15). The β1,3-N-acetylglucosaminyltransferase activity
  of Fringe proteins is essential for their biological activity in
  Drosophila (16-18) and in cell-based Notch signaling assays (19), and
  the O-fucose residues are required for Fringe to modulate Notch
  activity (16, 19). Thus, Fringe mediates its effects on Notch
  signaling by the addition of GlcNAc to O-fucose moieties. Nonetheless,
  neither the specific role ofO-fucose in Notch function nor the
  mechanism of how a change in sugar structure alters Notch function is
  known.