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solute carrier ( slc ) transporters are increasingly recognized as essential for ion , molecule , and other solute transport to support lysosomal function . to date , more than 30 lysosomal slc transporters have been genetically identified , molecularly characterized , and investigated for a role in health and disease . despite these advances , there remain lysosomal transport systems for which the molecular identity is obscure , and , conversely , orphan lysosomal slc transporters with functional relevance unresolved .
as the scope of lysosomal slc transporters is broad , expression , functional characteristics , and disease associations for known family members are summarized in table 
 1 .
instead , we focus on recent discoveries in the lysosomal slc transporter field that provide novel mechanistic insight into autophagy , phagocytosis , and exocytosis processes ( figure 
 1 ) .
major lysosomal solute carrier transporters cat1 , cationic amino acid transporter 1 ; cip1 , cationchloride cotransporterinteracting protein 1 ; ctr2 , copper transporter 2 ; dmt1 , divalent metal transporter 1 ; eaat2 , excitatory aminoacid transporter 2 ; ent3 , equilibrative nucleoside transporter ; fpn1 , ferroportin1 ; glut8 , glucose transporter 8 ; hrg1 , hemeresponsive gene 1 ; kbat , kidney brain anion transporter ; km , apparent substrate affinity lyaat1 , lysosomal amino acid transporter 1 ; matp , membraneassociated transporter protein ; mct12 , monocarboxylate transporter 12 ; nhe6 , sodium hydrogen exchanger ; nramp1 , natural resistanceassociated macrophage protein 1 ; pat1 , proton / amino acid transporter 1 ; pht1 , peptide histidine transporter 1 ; pht2 , peptide histidine transporter 2 ; snat7 , sodiumcoupled neutral amino acid transporter 7 ; spx2 , sugar phosphate exchanger 2 ; urlc11 , upregulated in lung cancer 11 ; viaat , vesicular inhibitory amino acid transporter ; vnut , vesicular nucleotide transporter ; zip8 , zinc transporter 8 ; znt2 , zinc transporter 2 . a schematic model of the lysosomal solute carrier ( slc)ome : emerging roles in cellular pathophysiology and pharmacology .
a multitude of lysosomal slcs across lysosomal membrane is involved in the lysosomal transport of solutes .
significant advances in understanding the lysosome proteome has revealed novel roles for lysosomal slcs , including slc38a9 as an amino acid sensor ( by direct interaction with mtor complex ) , slc17a9 as a mediator of adenosine triphosphate ( atp ) exocytosis , slc15a3/a4 as a participant in tolllike receptor ( tlr ) signaling , slc29a3 as a regulator of nucleoside salvage , and slc46a3 as a facilitator of antibodydrug conjugate maytansine efflux .
mtor , mammalian target of rapamycin ; raga , ragulator a ; ragc , ragulator c. distinct amino acid transport systems exist in the lysosomal membrane to transit cystine , cysteine , cationic amino acids , dicarboxylic amino acids , and small and large neutral amino acids , as elucidated over the last 3 decades .
similarly , the process of autophagy  lysosomal degradation of defective intracellular material during cellular stress 
was recognized well over 3 decades ago . yet , the mechanism for precisely relaying cellular nutrient status to lysosomes to regulate the autophagy process was unclear .
previous work predicted that the species and quantity of amino acids inside the lysosomal lumen were somehow sensed by the lysosome to allow docking of a master regulator of autophagy ( mammalian target of rapamycin complex 1 [ mtorc1 ] ) to the lysosomal surface to initiate an autophagy signal .
three groups have now independently discovered slc38a9 as an arginine sensor at the lysosomal membrane , identifying a central role for this transporter in regulating the steps preceding autophagy .
slc38a9 is an 11pass lysosomal transmembrane protein and a low capacity neutral amino acid transporter that directly interacts with ragulator 
ragulator gtpases conveying the nutrient status of the cell to the mtorc1 complex.1 the initiation and formation of doublemembraned autophagosomes tightly links mtorc1 regulation to this nutrientsensing mechanism . thus ,
identification of slc38a9 as an amino acid sensor was a critical step to understanding lysosomal signaling processes in autophagy .
it is not yet known whether additional amino acid sensors or analogous sensors for sugars , lipids , or nucleotides exist within or outside lysosomes , but these discoveries drive the quest to find new sensors for autophagy initiation and termination .
moreover , modulation of lysosomal slc38a9 transporters may offer a new therapeutic intervention in neurodegenerative and aging disorders in which autophagy is perturbed .
lysosomes also serve as the terminal compartment for cellular endocytic machinery and degradation of endocytosed material .
besides other functions , phagocytosis is essential for internalizing pathogens for degradation and for orchestrating immune responses .
the handling of pathogens by dendritic cells for the engagement of adaptive immune response is intricately tied to endolysosomal function . among lysosomal slc transporters
known to facilitate this process , the endolysosomal peptide transporters , slc15a3 and slc15a4 , in dendritic cells are reported to mediate the intracellular sensing of pathogens after tolllike receptor stimulation.2 both transporters assist in the egress of bacterially derived components , particularly muramyl dipeptide , to facilitate the nod2mediated immune response .
consistently , single nucleotide polymorphism of slc15a4 is found to associate with autoimmune disease systemic lupus erythematosus .
similarly , slc11a1 ( formerly nramp1 ) , a divalent metal transporter , is reported in dynamic hostpathogen interactions essential for conferring resistance to certain pathogens .
mutations in slc11a1 associate with infectious ( e.g. , tuberculosis , leprosy ) and inflammatory ( e.g. , rheumatoid arthritis ) diseases .
recently , the role of an acidic phdependent lysosomal nucleoside transporter , slc29a3 , has been linked to macrophage phagocytic function.3 slc29a3 is predicted to salvage lysosomal nucleobases , nucleosides , and nucleotides , presumably derived from encapsulated pathogens and host macrophagederived nucleic acids .
accumulating evidence reveals that slc29a3 mutations can cause a spectrum of human genetic disorders due to abnormal lysosomal nucleoside buildup and increased intralysosomal ph .
these diseases include : h syndrome ( progressive scleroderma , hyperpigmentation , hypertrichosis , facial telangiectases and dermal and subcutaneous fibrosis ) ; pigmented hypertrichotic dermatosis and insulindependent diabetes syndrome ; familial rosaidorfman disease ; familial histiocytosis ; and sinus histiocytosis with massive lymphadenopathy .
slc29a3 spectrum disorders are allelic , share common mutation(s ) , and share overlapping manifestations that display an intriguing resemblance to lysosomal storage disorders .
although the basis of these monogenic disorders is only beginning to be appreciated , further studies on the involvement of slc29a3 in lysosomal and cellular homeostasis should clarify the role of macrophages and other cell types in the pathogenesis of slc29a3 spectrum disorders .
the lysosome participates in membrane trafficking and exocytosis , wherein the lysosome expels its cargo outside the cell .
deficiency of lysosomal proteins in niemann  pick type c1 disease or niemann  pick type c2 diminish cholesterol efflux from the lysosomal compartment , leading to abnormal lysosomal cholesterol accumulation .
correspondingly , a recent finding identified slc17a9 in lysosomemediated adenosine triphosphate ( atp ) release.4 because atp is an important neurotransmitter , lysosomal exocytosis maintains regulated atp release from neurons and/or astrocytes .
atp facilitates synaptic efficiency and plasticity in neurons , and its dysregulation associates with central nervous system pathologies , including brain ischemia , inflammation , and stroke .
the localization of slc transporters on the lysosomal membrane represents a potential class of  druggable  targets for treating lysosomal disorders
. however , success , to date , is limited due to the initial requirement of endocytosis for drugs to reach the lysosome .
nevertheless , alternative strategies to effectively utilize or target lysosomal slcs for development of improved therapeutics are underway .
for instance , antibodydrug conjugates are emerging as a cancerspecific treatment to avoid offtarget toxicities observed with conventional chemotherapeutic agents . upon binding of antibodydrug conjugates to surface antigens on cancer cells ,
. however , the active drug now faces the impending challenge of finding its way out of the lysosome to reach its target site ( nucleus , cytoplasm , cytoskeleton , etc . ) for action .
because oligonucleotide ( sirna , mirna ) therapeutics and nanoparticlebased therapeutics face the same drugexit impediment , lysosomal accumulation and degradation have become a widespread concern .
cleavable linker technology , protonsponge effect , ion pair formation , and hydrophobic modification of vectors or cargos are some of the techniques being currently used for effective drug delivery . in some cases ,
regard , lysosomal slcs offer great promise to aid safe efflux of therapeutic cargos from lysosomes .
a recent discovery of slc46a3 facilitating transport of a noncleavable antibodydrug conjugate catabolite to export cargo from the lysosome validates the feasibility of this strategy.5 identification and characterization of orphan slc46a3 identified maytansine as a substrate for slc46a3 , further clarifying the mechanism of noncleavable maytansinebased antibody drug conjugates , including adotrastuzumab emtansine .
the discovery of slc46a3 as a means for antibodydrug conjugates to target cancer cells suggests future investigation will identify other lysosomal slc transporters with substrates amenable to therapeutic conjugation for lysosomal exit . in another example , slc31a2 , the lysosomal copper transporter , regulates sensitivity to cisplatin treatment .
measurement of copper flux with new intracellular copper sensors enables testing for copperdependent sensitivity to chemotherapeutic agents .
enhancement of transporter activity is a treatment option for diseases with loss of transporter function .
the lysosomal glutamate transporter , slc1a2 ( eaat2 ) , is involved in glutamate clearance in astroglial cells , and its protein expression decreases in neurological disorders , like alzheimer disease , amyotrophic lateral sclerosis , and schizophrenia . the antibiotic ceftriaxone increases transcription of slc1a2 through modulating nuclear factorkappa b signaling and riluzole , an amyotrophic lateral sclerosis therapeutic , reportedly increases transport activity of slc1a1 and slc1a2 , supporting this strategy .
furthermore , slc12a9 is a member of the sodium chloride cotransporter family ( slc12 ) that regulates ion gradients across renal tubules and maintains cell volume .
mutations in slc12a9 associate with bartter disease , characterized by a defect in the thick ascending limb of the loop of henle , hypokalemia , and alkalosis .
diuretic drugs , like bumetanide and furosemide , inhibit multiple slc12 transporters ; thus , directed development of novel diuretics that target specific slc12 transporters may offer more effective disease management .
finally , various lysosomal storage disorders are caused by an aberrant accumulation of undigested material within lysosomes .
classic examples involving lysosomal transporters include slc17a5 and mfsd8 in salla disease and neuronal ceroid lipofuscinosis , respectively .
although there are no curative treatments yet , enzyme replacement therapy and gene therapy are promising options . some treatment options for lysosomal storage disorders , like niemenpick disease , gaucher disease , and alphamannosidosis using enzyme replacement therapy are already approved or are under active ( pre)clinical evaluations .
overall , targeting and utilization of slc transporters for better treatment and management of lysosomal disorders or drug delivery is becoming a reality and research on lysosomal slcs is gaining momentum to realize new therapeutic possibilities .
emerging evidence indicates that lysosome function extends beyond macromolecular degradation . 
 genetic and functional defects in components of the lysosomal transport machinery cause lysosomal storage disorders implicating the lysosomal solute carrier ( slc ) transporters as essential to vital cell processes . 
 the pathophysiology and therapeutic potential of lysosomal slc transporters are highlighted here , focusing on recent discoveries in autophagic amino acid sensing ( slc38a9 ) , phagocytic regulation in macrophages ( slc29a3 , slc15a3/a4 ) , adenosine triphosphate ( atp ) exocytosis in neurotransmission ( slc17a9 ) , and lysosomal transport of maytansine catabolites into the cytoplasm ( slc46a3 ) .