Bark split into parallel ridges or sometimes smooth. Leaves and buds in 2 regular ranks, not crowded at the stem apex (except sometimes in leading [not lateral] stems of C. dentata). Buds 2–5 mm long, ovoid, rounded or bluntly pointed at the tip, with several overlapping scales, the 2 basal scales opposite, the others alternate, the terminal bud absent (the bud in the axil of the youngest leaf usually appears terminal). Stipules relatively large and prominent in spring, often shed early, herbaceous to papery, narrowly lanceolate to ovate. Leaf blades coarsely toothed, the secondary veins reaching the margin. Inflorescences staminate and pistillate or with pistillate flowers near the base and staminate flowers above them, the staminate catkins stiffly ascending or erect, elongate spikelike, the pistillate flowers sessile. Fruits ripening the first autumn after flowering. Cupules splitting into 2 or 4 valves, completely enclosing the nuts, spiny, the spines long and branched, crowded and hiding the surface of the cupule. Nuts 1–3 per cupule, more or less ovoid, sharply pointed at the tip and with a large attachment scar at the base, circular in cross-section or flattened on 1 or 2 sides, brown. About 10 species, eastern North America, Europe, Asia.

American chestnuts have been seriously impacted by chestnut blight, caused by an Asiatic fungus, Cryphonectria parasitica (Murrill) Barr. This disease was introduced into the United States during the late 1800s through nursery stock from Asia and was first reported to be killing trees in New York around 1904 (Burnham, 1988). All of the native chestnuts are very susceptible to the blight, and it spread rapidly through the eastern United States. Infected trees are typically killed down to ground level. The root system remains unaffected, and blighted trees may repeatedly resprout from the roots, the stems growing until they are reinfected and dying back again (Paillet, 1993). However, over successive diebacks and resproutings, the progressively weakened plants eventually perish. Burnham (1988) summarized efforts by the American Chestnut Society and other scientists to restore C. dentata by hybridizing plants with various Asian chestnut species and then repeatedly backcrossing the progeny to the American chestnut parent over several generations to produce a blight resistant tree with mostly a C. dentata genome. Other studies have focused on locating a less virulent form of the fungus to act as a biological control for chestnut blight. More recently, similar studies have begun through the Ozark Chinquapin Foundation and others with the intent of producing a disease resistant form of C. pumila.