Negatively regulates the activity of members of the MAP kinase family in response to changes in the cellular environment. Has a specificity for the ERK family. Acts as negative regulator in a variety of developmental processes including cell differentiation and proliferation controlled by the Ras/ERK pathway. Suppresses the photoreceptor cell differentiation and wing vein formation. Required for proper oogenesis and early embryogenesis. Functions autonomously in a subset of photoreceptor progenitor cells in eye imaginal disks. Appears also to be required in surrounding non-neuronal cells for ommatidial patterning and photoreceptor differentiation. Plays a role in the maintenance of epithelial integrity during tracheal development. H2O + O-phospho-L-tyrosyl-[protein] = L-tyrosyl-[protein] + phosphate H2O + O-phospho-L-seryl-[protein] = L-seryl-[protein] + phosphate H2O + O-phospho-L-threonyl-[protein] = L-threonyl-[protein] + phosphate Activity abolished by tyrosine phosphatase inhibitor sodium vanadate. Activated by rl. Interacts (via N-terminal region) with phosphorylated rl. Ubiquitous expression in eye and wing imaginal disks. Enriched in ovary. Low expression in the various developmental stages, although relatively high levels detected in 8 to 12 h embryos, as well as in pupae and adults, particularly in the head region. Expressed in third-instar eye imaginal disks posterior to the morphogenetic furrow where photoreceptor differentiation occurs. Preferentially detected in wing imaginal disks in two stripes of cells interrupted at the dorsoventral boundary, which correspond to the developing veins L3 and L4. In pupal wings the maximal levels of expression are present in all longitudinal veins, with low levels detected in most intervein cells. Uniformly distributed in the syncytial blastoderm (stage 4). At early stage 5, accumulates at the embryonic poles and is absent from the central region. This pattern evolves very rapidly with the formation of a third central domain of expression from 85% to 40% egg length. In older embryos, the main places where high levels accumulate correspond to the invaginating mesoderm, the tracheal pits at stage 11, the visceral mesoderm at stage 13, the heart, the midline and the apodema. Expression in tracheal branches at later stages. Homozygous embryonic lethal, while hypomorphic alleles (reduction in gene dosage) lead to extra photoreceptor cells in the eye, ectopic veins in wings and severe defects in oogenesis in females. Females with the germ line mutation lay only a small number of eggs. The laid eggs are abnormal, approximately 77% of the laid eggs are shorter and some display severe defects in chorion formation. These embryos could not escape the embryonic stage and progress beyond the two-nuclei stage. Null mutants are viable and fertile exhibiting a mild, but significant increase in wing vein material. They are slightly rough eyed. Null mutation affects the R3 and R4 photoreceptors with a low penetrance resulting in either the loss of one cell of the R3/R4 pair or in the misdifferentiation of these photoreceptors. R3 and R4 are often symmetrically arranged in the eye in opposite to the asymmetrical positions they adopt in wild-type ommatidium. Ommatidia of the null mutants often contain a mystery cell having differentiated as a photoreceptor. Null mutants also exhibit mild delay in tracheal branching. Delay in 12% dorsal branches (DBs) compared with 0.3% in wild-type between metameres 4 to 8 that have reached the dorsal midline at stage 14-15. Null mutants have defects in cell intercalation. Belongs to the protein-tyrosine phosphatase family. Non-receptor class dual specificity subfamily. Extended N-terminus.