v1.8.0: SOD1-G93A time course and disease-state cell source (Amendment 14)

Adds Amendment 14: a spatial time course in SOD1-G93A mice, a third human spatial cohort, and the disease-state cell source of the module genes in human spinal cord.

New in v1.8.0

• Amendment 14 (docs/analysis_plans/..._AMENDMENT_14.md), committed before W71 and W72 were run.
• W71: Maniatis et al. 2019 ALS-ST data
  • Scripts: build_w71_maniatis_pseudobulk.py, run_w71_mouse_time_course.R, run_w71_human_colocalisation.py.
  • Mouse, SOD1-G93A vs SOD1-WT lumbar cord, ventral vs dorsal horn at P30, P70, P100 and P120. Only 2-4 module orthologs are testable, so the mouse module is mainly C3.
    • Cross-species replication reading: nominal (P100 interaction P = 0.043, BH = 0.17).
    • Timing reading: symptomatic or late. There is no change at P30 or P70; the rise starts in the ventral horn at P100 and extends to the dorsal horn at P120.
  • Human: seven ALS patients, no controls, so analysis is descriptive. The module score correlates most with microglial scores, but weakly.
• W72: disease-state lineage share in GSE287257
  • Scripts: run_w72_zelic_disease_cell_source.py, run_w72_lineage_de.R.
  • GPNMB (74%) and C3 (81%) come mainly from microglia in ALS spinal cord, LTF from astrocytes, and ANXA1 and EMP3 from vascular cells.
  • ALS also raises GPNMB and C3 in astrocytes.
• scripts/figures_v2/figS10_mouse_cell_source.R: new Supplementary Fig. S10. The Fig. 1 timeline is updated.
• Supplementary Tables:
  • S1: Amendment 14.
  • S2: W71 tests, 482 rows in total.
  • S3: one implementation detail.
  • S4: new sheets S4n-S4q.
• README (data source and pipeline) and CITATION (v1.8.0) updated.

The Maniatis data come from the ALS-ST portal (https://als-st.nygenome.org); see the README for the expected folder layout. No data are included.